Passive Head Rotation Research Articles

Eye position dependency of nystagmus during constant vestibular stimulation

Alexander's law, the eye position dependency of nystagmus due to peripheral vestibular lesions, has been hypothesized to occur due to adaptive changes in the brainstem velocity-to-position neural integrator in response to non-reciprocal vestibular stimulation. We investigated whether it develops during passive head rotations that produce constant nystagmus for >35 s. The yaw rotation stimulus consisted of a 1-s acceleration (100°/s(2)), followed by a lower acceleration ramp (starting at 7.3°/s(2) and increasing at 0.04°/s(2)/s) until 400°/s was reached after 38 s. This stimulus was designed to offset the ~15 s vestibular ocular reflex time constant (and the 150 s adaptation time constant) and produce constant velocity slow phases. In contrast to peripheral lesions, this vestibular stimulation is the result of real head turns and has the push-pull characteristics of natural movements. The procedure was successful, as the average velocity of 31°/s was unchanged over the final 35 s of the acceleration period. In all 10 healthy human subjects, we found a large and stable Alexander's law, with an average velocity-versus-position slope of -0.366 in the first half that was not significantly different in the second half, -0.347. These slopes correspond to integrator time constants of <3 s, are much less than normal time constants (~25 s), and are similar to those observed in patients with peripheral vestibular lesions. Alexander's law also developed, on average, in 10 s. We conclude that Alexander's law is not simply a consequence of non-reciprocal vestibular stimulation.

In vivo three-dimensional kinematics of the cervical spine during maximal axial rotation

The cervical spine exhibits considerable mobility, especially in axial rotation. Axial rotation exerts stress on anatomical structures, such as the vertebral artery which is commonly assessed during clinical examination. The literature is rather sparse concerning the in vivo three-dimensional segmental kinematics of the cervical spine. This study aimed at investigating the three-dimensional kinematics of the cervical spine during maximal passive head rotation with special emphasis on coupled motion. Twenty healthy volunteers participated in this study. Low-dose CT scans were conducted in neutral and in maximum axial rotation positions. Each separated vertebra was segmented semi automatically in these two positions. The finite helical-axis method was used to describe 3D motion between discrete positions. The mean (±SD) maximum magnitude of axial rotation between C0 and C1 was 2.5 ± 1.0° coupled with lateral flexion to the opposite side (5.0 ± 3.0°) and extension (12.0 ± 4.5°). At the C1–C2 level, the mean axial rotation was 37.5 ± 6.0° associated with lateral flexion to the opposite side (2.5 ± 6.0°) and extension (4.0 ± 6.0°). For the lower levels, axial rotation was found to be maximal at C4–C5 level (5.5 ± 1.0°) coupled with lateral flexion to the same side (−4.0 ± 2.5°). Extension was associated at levels C2–C3, C3–C4 and C4–C5, whereas flexion occurred between C5–C6 and C6–C7. Coupled lateral flexion occurred to the opposite side at the upper cervical spine and to the same side at the lower cervical spine.

False-Positive Head-Impulse Test in Cerebellar Ataxia

The objective of this study was to compare the findings of the bedside head-impulse test (HIT), passive head rotation gain, and caloric irrigation in patients with cerebellar ataxia (CA). In 16 patients with CA and bilaterally pathological bedside HIT, vestibuloocular reflex (VOR) gains were measured during HIT and passive head rotation by scleral search coil technique. Eight of the patients had pathologically reduced caloric responsiveness, while the other eight had normal caloric responses. Those with normal calorics showed a slightly reduced HIT gain (mean ± SD: 0.73 ± 0.15). In those with pathological calorics, gains 80 and 100 ms after the HIT as well as the passive rotation VOR gains were significantly lower. The corrective saccade after head turn occurred earlier in patients with pathological calorics (111 ± 62 ms after onset of the HIT) than in those with normal calorics (191 ± 17 ms, p = 0.0064). We identified two groups of patients with CA: those with an isolated moderate HIT deficit only, probably due to floccular dysfunction, and those with combined HIT, passive rotation, and caloric deficit, probably due to a peripheral vestibular deficit. From a clinical point of view, these results show that the bedside HIT alone can be false-positive for establishing a diagnosis of a bilateral peripheral vestibular deficit in patients with CA.

Absence of compensation for vestibular-evoked passive head rotations in human sound localization

A world-fixed sound presented to a moving head produces changing sound-localization cues, from which the audiomotor system could infer sound movement relative to the head. When appropriately combined with self-motion signals, sound localization remains spatially accurate. Indeed, free-field orienting responses fully incorporate intervening eye-head movements under open-loop localization conditions. Here we investigate the default strategy of the audiomotor system when localizing sounds in the absence of efferent and proprioceptive head-movement signals. Head- and body-restrained listeners made saccades in total darkness toward brief (3, 10 or 100 ms) broadband noise bursts, while being rotated sinusoidally (f=1/9 Hz, V(peak) =112 deg/s) around the vertical body axis. As the loudspeakers were attached to the chair, the 100 ms sounds might be perceived as rotating along with the chair, and localized in head-centred coordinates. During 3 and 10 ms stimuli, however, the amount of chair rotation remained well below the minimum audible movement angle. These brief sounds would therefore be perceived as stationary in space and, as in open-loop gaze orienting, expected to be localized in world-centred coordinates. Analysis of the saccades shows, however, that all stimuli were accurately localized on the basis of imposed acoustic cues, but remained in head-centred coordinates. These results suggest that, in the absence of motor planning, the audio motor system keeps sounds in head-centred coordinates when unsure about sound motion relative to the head. To that end, it ignores vestibular canal signals of passive-induced head rotation, but incorporates intervening eye displacements from vestibular nystagmus during the saccade-reaction time.

Characterizing high-velocity angular vestibulo-ocular reflex function in service members post-blast exposure

Blasts (explosions) are the most common mechanism of injury in modern warfare. Traumatic brain injury (TBI) and dizziness are common sequelae associated with blasts, and many service members (SMs) report symptoms worsen with activity. The purpose of this study was to measure angular vestibulo-ocular reflex gain (aVOR) of blast-exposed SMs with TBI during head impulse testing. We also assessed their symptoms during exertion. Twenty-four SMs recovering from TBI were prospectively assigned to one of two groups based on the presence or absence of dizziness. Wireless monocular scleral search coil and rate sensor were used to characterize active and passive yaw and pitch head and eye rotations. Visual analog scale (VAS) was used to monitor symptoms during fast walking/running. For active yaw head impulses, aVOR gains were significantly lower in the symptomatic group (0.79±0.15) versus asymptomatic (0.87±0.18), but not for passive head rotation. For pitch head rotation, the symptomatic group had both active (0.915±0.24) and passive (0.878±0.22) aVOR gains lower than the asymptomatic group (active 1.03±0.27, passive 0.97±0.23). Some SMs had elevated aVOR gain. VAS scores for all symptoms were highest during exertion. Our data suggest symptomatic SMs with TBI as a result of blast have varied aVOR gain during high-velocity head impulses and provide compelling evidence of pathology affecting the vestibular system. Potential loci of injury in this population include the following: disruption of pathways relaying vestibular efference signals, differential destruction of type I vestibular hair cells, or selective damage to irregular afferent pathways-any of which may explain the common discrepancy between reports of vestibular-like symptoms and laboratory testing results. Significantly reduced pitch aVOR in symptomatic SMs and peak symptom severity during exertional testing support earlier findings in the chronic blast-exposed active duty SMs.

A New Dynamic Visual Acuity Test to Assess Peripheral Vestibular Function

To evaluate a novel test for dynamic visual acuity (DVA) that uses an adaptive algorithm for changing the size of Landolt rings presented during active or passive head impulses, and to compare the results with search-coil head impulse testing. Prospective study in healthy individuals and patients with peripheral vestibular deficits. Tertiary academic center. One hundred neuro-otologically healthy individuals (age range, 19-80 years) and 15 patients with bilateral (n = 5) or unilateral (n = 10) peripheral vestibular loss (age range, 27-72 years). Testing of static visual acuity (SVA), DVA during active and passive horizontal head rotations (optotype presentation at head velocities >100 degrees/s and >150 degrees/s), and quantitative horizontal head impulse testing with scleral search coils. Difference between SVA and DVA, that is, visual acuity loss (VA loss), gain of the high-acceleration vestibulo-ocular reflex. Passive head impulses and higher velocities were more effective than active impulses and lower velocities. Using passive head impulses and velocities higher than 150 degrees/s, the DVA test discriminated significantly (P < .001) among patients with bilateral vestibulopathy, those with unilateral vestibulopathy, and normal individuals. The DVA test sensitivity was 100%, specificity was 94%, and accuracy was 95%, with search-coil head impulse testing used as a reference. In healthy individuals, VA loss increased significantly with age (P < .001; R(2) = 0.04). Dynamic visual acuity testing with Landolt rings that are adaptively changed in size enables detection of peripheral vestibular dysfunction in a fast and simple way.

Oculomotor Strategies and Their Effect on Reducing Gaze Position Error

Vestibular adaptation exercises have been shown to improve gaze stability during active head rotation in individuals with vestibular hypofunction. Little is known, however, of the types of eye movements used during passive head rotation and their effect on gaze stability in individuals with vestibular hypofunction. The primary purpose of this study was to determine differences in oculomotor strategies and their effect on stabilizing gaze during ipsilesional passive and active head rotations in vestibular hypofunction. Subjects with unilateral (n = 4) and bilateral (n = 3) vestibular hypofunction and healthy subjects (n = 4) based on bithermal caloric and rotational chair testing. Diagnostic. Head and eye velocity and position data measured with scleral search coil. Subjects with unilateral and bilateral vestibular hypofunction generated 3 types of gaze-stabilizing eye movements with ipsilesional head impulses: slow vestibular ocular reflex, compensatory, and corrective saccades. The types of eye movements generated during active and passive head impulses were highly individualized. Gaze position error was reduced when compensatory saccades were recruited as part of the gaze-stabilizing strategy. Rehabilitation for individuals with vestibular hypofunction should identify individuals' unique gaze stability preferences and attempt to facilitate compensatory saccades.

Effects of canal plugging on the vestibuloocular reflex and vestibular nerve discharge during passive and active head rotations.

Mechanical occlusion (plugging) of the slender ducts of semicircular canals has been used in the clinic as well as in basic vestibular research. Here, we investigated the effect of canal plugging in two macaque monkeys on the horizontal vestibuloocular reflex (VOR) and the responses of vestibular-nerve afferents during passive head rotations. Afferent responses to active head movements were also studied. The horizontal VOR gain decreased after plugging to <0.1 for frequencies <2 Hz but rose to about 0.6 as frequency was increased to 15 Hz. Afferents innervating plugged horizontal canals had response sensitivities that increased with the frequency of passive rotations from <0.01 (spikes/s)/( degrees/s) at 0.5 Hz to values of about 0.2 and 0.5 (spikes/s)/( degrees/s) at 8 Hz for regular and irregular afferents, respectively (<50% of responses in controls). An increase in phase lead was also noted following plugging in afferent discharge, but not in the VOR. Because the phase discrepancy between the VOR and afferent discharge is much larger than that seen in control animals, this suggests that central adaptation shapes VOR dynamics following plugging. The effect of canal plugging on afferent responses can be modeled as an increase in stiffness and a reduction in the dominant time constant and gain in the transfer function describing canal dynamics. Responses were also evident during active head rotations, consistent with the frequency content of these movements. We conclude that canal plugging in macaques is effective only at frequencies <2 Hz. At higher frequencies, afferents show significant responses, with a nearly 90 degrees phase lead, such that they encode near-rotational acceleration. Our results demonstrate that afferents innervating plugged canals respond robustly during voluntary movements, a finding that has implications for understanding the effects of canal plugging in clinical practice.

Reafferent Head-Movement Signals Carried by Pursuit Neurons of the Simian Frontal Eye Fields during Head Movements

The smooth-pursuit system is important to precisely track a slowly moving object and maintain its image on the foveae during movement. During whole-body rotation, the smooth-pursuit system interacts with the vestibular system. The caudal part of the frontal eye fields (FEF) contains smooth pursuit-related neurons that signal eye velocity during pursuit. The majority of them receives vestibular inputs and signal gaze-velocity during passive whole-body rotation. It was asked whether discharge modulation of FEF pursuit neurons during head rotation on the stationary trunk could be accounted for by vestibular inputs only or if both vestibular and neck proprioceptive inputs contributed to the modulation. Discharge modulation during active head pursuit, passive head rotation on the stationary trunk, passive whole-body rotation, and passive trunk rotation against the stationary head were compared. The results indicate that both vestibular and neck proprioceptive inputs contributed to the discharge modulation of FEF pursuit neurons during head movements.

Impulsive Testing of Semicircular‐Canal Function Using Video‐oculography

The head impulse test (HIT) is a safe, quick way of assessing horizontal semicircular-canal function in patients with peripheral vestibular loss. At the bedside, the clinician identifies "overt" catch-up saccades back to the target after brisk passive head rotation as an indirect sign of canal paresis. However, saccades during head rotation ("covert" saccades) may not be detectable by the naked eye, and so lead to incorrect diagnosis. Up to now, the scleral search coil technique has been the standard for HIT measurement, but that technique is not practical for routine diagnostic use. A new lightweight, nonslip, high-speed video-oculography system (vHIT) that measures eye velocity during horizontal head impulses has been developed. This system is easy to use in a clinical setting, provides an objective measure of the vestibulo-ocular reflex (VOR), and detects both overt and covert catch-up saccades in patients with vestibular loss.

Neck rigidity in Parkinson's disease patients is related to incomplete suppression of reflexive head stabilization

Muscle rigidity in PD (Parkinson's disease) patients represents an involuntary increase in muscle tone that stands out upon passive rotation of a joint. The pathophysiology of rigidity is still not well understood. We measured head–trunk torque in PD patients and normal controls during transient passive head rotations by means of servomotors under the instruction to the subjects to relax the neck muscles. We observed that rotation onset was followed by an initial rapid rise in resistive torque, similarly in both subject groups. It then leveled off or declined in controls. With PD patients, in contrast, the rise continued roughly proportional to head eccentricity almost until the end of the rotation. These observations led us to the hypothesis that the initial rise in torque represents reflexive head stabilization that normal subjects in the course of the rotational stimulus are able to suppress, whereas PD patients are less effective in doing so. The hypothesis was implemented into a dynamic control model of active and passive head rotation. Model simulations successfully reproduced the torque responses of normal subjects and PD patients in the present and previous studies.

Eye-Pursuit and Reafferent Head Movement Signals Carried by Pursuit Neurons in the Caudal Part of the Frontal Eye Fields during Head-Free Pursuit

Eye and head movements are coordinated during head-free pursuit. To examine whether pursuit neurons in frontal eye fields (FEF) carry gaze-pursuit commands that drive both eye-pursuit and head-pursuit, monkeys whose heads were free to rotate about a vertical axis were trained to pursue a juice feeder with their head and a target with their eyes. Initially the feeder and target moved synchronously with the same visual angle. FEF neurons responding to this gaze-pursuit were tested for eye-pursuit of target motion while the feeder was stationary and for head-pursuit while the target was stationary. The majority of pursuit neurons exhibited modulation during head-pursuit, but their preferred directions during eye-pursuit and head-pursuit were different. Although peak modulation occurred during head movements, the onset of discharge usually was not aligned with the head movement onset. The minority of neurons whose discharge onset was so aligned discharged after the head movement onset. These results do not support the idea that the head-pursuit–related modulation reflects head-pursuit commands. Furthermore, modulation similar to that during head-pursuit was obtained by passive head rotation on stationary trunk. Our results suggest that FEF pursuit neurons issue gaze or eye movement commands during gaze-pursuit and that the head-pursuit–related modulation primarily reflects reafferent signals resulting from head movements.

Human Updating of Visual Motion Direction During Head Rotations

Previous studies have demonstrated that human subjects update the location of visual targets for saccades after head and body movements and in the absence of visual feedback. This phenomenon is known as spatial updating. Here we investigated whether a similar mechanism exists for the perception of motion direction. We recorded eye positions in three dimensions and behavioral responses in seven subjects during a motion task in two different conditions: when the subject's head remained stationary and when subjects rotated their heads around an anteroposterior axis (head tilt). We demonstrated that after head-tilt subjects updated the direction of saccades made in the perceived stimulus direction (direction of motion updating), the amount of updating varied across subjects and stimulus directions, the amount of motion direction updating was highly correlated with the amount of spatial updating during a memory-guided saccade task, subjects updated the stimulus direction during a two-alternative forced-choice direction discrimination task in the absence of saccadic eye movements (perceptual updating), perceptual updating was more accurate than motion direction updating involving saccades, and subjects updated motion direction similarly during active and passive head rotation. These results demonstrate the existence of an updating mechanism for the perception of motion direction in the human brain that operates during active and passive head rotations and that resembles the one of spatial updating. Such a mechanism operates during different tasks involving different motor and perceptual skills (saccade and motion direction discrimination) with different degrees of accuracy.

Mechanism of Dynamic Visual Acuity Recovery With Vestibular Rehabilitation

Schubert MC, Migliaccio AA, Clendaniel RA, Allak A, Carey JP. Mechanism of dynamic visual acuity recovery with vestibular rehabilitation. Objective To determine why dynamic visual acuity (DVA) improves after vestibular rehabilitation in people with vestibular hypofunction. Design Combined descriptive and intervention study. Setting Outpatient department in an academic medical institution. Participants Five patients (age, 42–66y) and 4 age-matched controls (age, 39–67y) were studied. Patients had vestibular hypofunction (mean duration, 177±188d) identified by clinical (positive head thrust test, abnormal DVA), physiologic (reduced angular vestibulo-ocular reflex [aVOR] gain during passive head thrust testing), and imaging examinations (absence of tumor in the internal auditory canals or cerebellopontine angle). Intervention Vestibular rehabilitation focused on gaze and gait stabilization (mean, 5.0±1.4 visits; mean, 66±24d). The control group did not receive any intervention. Main Outcome Measures aVOR gain (eye velocity/head velocity) during DVA testing (active head rotation) and horizontal head thrust testing (passive head rotation) to control for spontaneous recovery. Results For all patients, DVA improved (mean, 51%±25%; range, 21%–81%). aVOR gain during the active DVA test increased in each of the patients (mean range, 0.7±0.2 to 0.9±0.2 [35%]). aVOR gain during passive head thrust did not improve in 3 patients and improved only partially in the other 2. For control subjects, aVOR gain during DVA was near 1. Conclusions Our data suggest that vestibular rehabilitation increases aVOR gain during active head rotation independent of peripheral aVOR gain recovery.

Response of Vestibular-Nerve Afferents to Active and Passive Rotations Under Normal Conditions and After Unilateral Labyrinthectomy

We investigated the possible contribution of signals carried by vestibular-nerve afferents to long-term processes of vestibular compensation after unilateral labyrinthectomy. Semicircular canal afferents were recorded from the contralesional nerve in three macaque monkeys before [horizontal (HC) = 67, anterior (AC) = 66, posterior (PC) = 50] and 1-12 mo after (HC = 192, AC = 86, PC = 57) lesion. Vestibular responses were evaluated using passive sinusoidal rotations with frequencies of 0.5-15 Hz (20-80 degrees /s) and fast whole-body rotations reaching velocities of 500 degrees /s. Sensitivities to nonvestibular inputs were tested by: 1) comparing responses during active and passive head movements, 2) rotating the body with the head held stationary to activate neck proprioceptors, and 3) encouraging head-restrained animals to attempt to make head movements that resulted in the production of neck torques of < or =2 Nm. Mean resting discharge rate before and after the lesion did not differ for the regular, D (dimorphic)-irregular, or C (calyx)-irregular afferents. In response to passive rotations, afferents showed no change in sensitivity and phase, inhibitory cutoff, and excitatory saturation after unilateral labyrinthectomy. Moreover, head sensitivities were similar during voluntary and passive head rotations and responses were not altered by neck proprioceptive or efference copy signals before or after the lesion. The only significant change was an increase in the proportion of C-irregular units postlesion, accompanied by a decrease in the proportion of regular afferents. Taken together, our findings show that changes in response properties of the vestibular afferent population are not likely to play a major role in the long-term changes associated with compensation after unilateral labyrinthectomy.

Illusory changes in head position induced by neck muscle vibration can alter the perception of elbow position.

Acuity for elbow joint position sense (JPS) is reduced when head position is modified. Movement of the head is associated with biomechanical changes in the neck and shoulder musculoskeletal system, which may explain changes in elbow JPS. The present study aimed to determine whether elbow JPS is also influenced by illusory changes in head position. Simultaneous vibration of sternocleidomastoid (SCM) and the contralateral splenius was applied to 14 healthy adult human subjects. Muscle vibration or passive head rotation was introduced between presentation and reproduction of a target elbow position. Ten out of 14 subjects reported illusions consistent with lengthening of the vibrated muscles. In these 10 subjects, absolute error for elbow JPS increased with left SCM/right splenius vibration but not with right SCM/left splenius vibration. Absolute error also increased with right rotation, with a trend for increased error with left rotation. These results demonstrated that both actual and illusory changes in head position are associated with diminished acuity for elbow JPS, suggesting that the influence of head position on upper limb JPS depends, at least partially, on perceived head position.

Behavior of the Position Vestibular Pause (PVP) Interneurons of the Vestibuloocular Reflex During Head-Free Gaze Shifts in the Monkey

Most behavioral studies indicate that the efficacy (gain) of the vestibuloocular reflex (VOR) in primates is modulated during the voluntary head movements that accompany large shifts in the direction of gaze. However, the timing and degree of this modulation is the subject of some debate. The neurophysiological substrate for this apparent gain reduction has been sought in the behavior of the type I position vestibular pause (PVP) neuron, a well-known type of interneuron in the direct VOR pathway. With the head fixed, PVPs increase their firing rates with contraversive eye position and with ipsiversive passive head rotation and also cease firing (pause) for the duration of ipsiversive saccades. During head-free ipsiversive gaze shifts, the eyes and head move in the same direction. If the vestibular signal carried by PVPs provides the primary drive for the VOR, the vestibular signal should be present during ipsiversive gaze shifts to the degree that the VOR is present. Of 25 type I PVPs recorded, 21 ceased their discharge for the entire duration of the rapid, eye-saccade component of an ipsiversive gaze shift. The resumption of activity occurred, on average, 13 ms after the end of the saccade. These results suggest that the activity of the vast majority of PVP neurons do not reflect the state of the VOR, but rather PVPs are completely eliminated from participation in the reflex during head-free gaze movements. We conclude that if any modulation of the VOR does exist, it must occur through other, probably longer-latency, pathways.

Electromyographic Activity of Dorsal Neck Muscles in Squirrel Monkeys During Rotations in an Upright or Upside Down Posture

Electromyographic (EMG) activity was recorded from occipitoscapularis, semispinalis, and splenius neck muscles in five alert squirrel monkeys during 0.25-Hz rotations about horizontal axes oriented at 22.5 degrees intervals, including pitch, roll, and intermediate axes. The animals were oriented in either upright or upside down posture. In the upright posture, all monkeys exhibited compensatory EMG activity with maximal activation during rotations about axes between pitch in the pitch forward direction and contralaterally directed roll. Response timing varied across animals with EMG peaks ranging from near pitch forward head velocity to near pitch forward head position. When the head was upside down, response dynamics and directionality were altered to varying degrees in different monkeys. The greatest change in response to head inversion was seen in the monkey that had response phases closest to head position, the least in the animal with phases closest to head velocity. The monkey with EMG response peaks closest to position phase showed nearly 180 degrees inversion of responses when the head was upside down, suggesting that in this monkey a righting reflex mediated by utricular signals was activated in the upside down posture. The monkey with EMG response peaks closest to velocity phase may have lacked a righting response and exhibited only a canal-mediated compensatory vestibulocervical reflex in both upright and upside down postures. The results suggest that reflex contraction of neck muscles in response to passive head rotation includes an interplay of compensatory and righting responses that varies from animal to animal.

Human 3-D aVOR with and without otolith stimulation

We describe in detail the frequency response of the human three-dimensional angular vestibulo-ocular response (3-D aVOR) over a frequency range of 0.05-1 Hz. Gain and phase of the human aVOR were determined for passive head rotations in the dark, with the rotation axis either aligned with or perpendicular to the direction of gravity (earth-vertical or earth-horizontal). In the latter case, the oscillations dynamically stimulated both the otolith organs and the semi-circular canals. We conducted experiments in pitch and yaw, and compared the results with previously-published roll data. Regardless of the axis of rotation and the orientation of the subject, the gain in aVOR increased with frequency to about 0.3 Hz, and was approximately constant from 0.3 to 1 Hz. The aVOR gain during pitch and yaw rotations was larger than during roll rotations. Otolith and canal cues combined differently depending upon the axis of rotation: for torsional and pitch rotations, aVOR gain was higher with otolith input; for yaw rotations the aVOR was not affected by otolith stimulation. There was a phase lead in all three dimensions for frequencies below 0.3 Hz when only the canals were stimulated. For roll and pitch rotations this phase lead vanished with dynamic otolith stimulation. In contrast, the horizontal phase showed no improvement with additional otolith input during yaw rotations. The lack of a significant otolith contribution to the yaw aVOR was observed when subjects were supine, prone or lying on their sides. Our results confirm studies with less-natural stimuli (off-vertical axis rotation) that the otoliths contribute a head-rotation signal to the aVOR. However, the magnitude of the contribution depends on the axis of rotation, with the gain in otolith-canal cross-coupling being smallest for yaw axis rotations. This could be because, in humans, typical yaw head movements will stimulate the otoliths to a much lesser extent then typical pitch and roll head movements.

Eye-head coordination in darkness: Formulation and testing of a mathematical model

Passive head rotation in darkness produces vestibular nystagmus, consisting of slow and quick phases. The vestibulo-ocular reflex produces the slow phases, in the compensatory direction, while the fast phases, in the same direction as head rotation, are of saccadic origin. We have investigated how the saccadic components of the ocular motor responses evoked by active head rotation in darkness are generated, assuming the only available sensory information is that provided by the vestibular system. We recorded the eye and head movements of nine normal subjects during active head rotation in darkness. Subjects were instructed to rotate their heads in a sinusoidal-like manner and to focus their attention on producing a smooth head rotation. We found that the desired eye position signal provided to the saccadic mechanism by the vestibular system may be modeled as a linear combination of head velocity and head displacement information. Here we present a mathematical model for the generation of both the slow and quick phases of vestibular nystagmus based on our findings. Simulations of this model accurately fit experimental data recorded from subjects.