Angular Vestibulo-ocular Reflex Research Articles

Adaptation of the angular vestibulo-ocular reflex to head movements in rotating frames of reference

Head movements in a rotating frame of reference are commonly encountered, but their long term effects on the angular vestibulo-ocular reflex (aVOR) are not well understood. To study this, monkeys were oscillated about a naso-occipital (roll) axis for several hours while rotating about a spatial vertical axis (roll-while-rotating, RWR). This induced oscillations in roll and pitch eye velocity and continuous horizontal (yaw) nystagmus. For several hours thereafter, simple roll in darkness induced horizontal nystagmus and pitch and roll oscillations. The rising and falling time constants of the horizontal velocity indicated that the nystagmus arose in velocity storage. The continuous nystagmus was correlated with a phase shift of vertical eye velocity from 90 degrees to 0 degrees re head position. As the phases reverted toward pre-adaptive values, the horizontal velocity declined. Similar yaw nystagmus and pitch and roll velocities were produced by oscillation in roll after adaptation with roll and horizontal optokinetic nystagmus (OKN), but not after adaptation with pitch-while-rotating (PWR). Findings were explained by a model that shifted the roll orientation vector of velocity storage toward the pitch axis during adaptation with RWR and Roll & OKN. This shift produced modulation in vertical eye velocity in the post adaptive state, which was approximately in phase with roll head position, generating horizontal nystagmus. Similar orientation changes to prolonged exposure to complex motion environments may be responsible for producing post-stimulus motion sickness and/or mal de debarquement.

Modification of the Cervico-ocular Reflex by Canal Plugging

The cervico-ocular reflex (COR) has a low gain in normal animals. In this study, we determined whether COR gain increases were specific to the low/midband frequency range, which is the range over which the angular vestibulo-ocular reflex (aVOR) is compromised by plugging. The gain and phase of the yaw and pitch COR and aVOR were compared in normal monkeys and those with all six semicircular canals or only the lateral canal plugged. During experiments animals sat with the body fixed to a chair and the head fixed in space. The body was oscillated about body-yaw and body-pitch axes over a frequency range of 0.05-6 Hz, with amplitude <10 degrees. For normal animals, both yaw and pitch eye velocities were compensatory to the relative velocity of the head with respect to the body. The gains were 0.1-0.2 at frequencies below 1 Hz and decreased to zero as stimulus frequency increased above 1 Hz. Canal-plugged animals had COR gains close to 1.0 at low frequencies, decreasing to approximately 0.6 at 0.5 Hz and to 0.2 for stimulus frequencies above 3 Hz. The phase of eye velocity was 180 degrees relative to head-re-body velocity at frequencies below 0.5 Hz and shifted toward 270 degrees as frequencies were increased to 4 Hz. This study demonstrates that adaptation of COR gain is tuned to a frequency range at which the aVOR is compromised by the canal plugging.

Effect of Canal Plugging on Quadrupedal Locomotion in Monkey

The vestibular system plays an important role in controling gait, but where in the labyrinths relevant activity arises is largely unknown. After the semicircular canals are plugged, low frequency (0.01-2 Hz) components of the angular vestibulo-ocular reflex (aVOR) and angular vestibulo-collic reflex (aVCR) are lost, but high frequency (3-20 Hz) components remain. We determined how loss of low frequency canal afference affects limb and head movements during quadrupedal locomotion. Head, body, and limb movements were recorded in three dimensions (3-D) in a cynomolgus monkey with a motion detection system, while the animal walked on a treadmill. All six canals were plugged, reducing the canal time constants from approximately 4.0 sec to approximately 0.07 sec. Major changes in the control of the limbs occurred after surgery. Fore and hind limbs were held farther from the body, producing a broad-based gait. Swing-phase trajectories were inaccurate, and control of medial-lateral limb movement was erratic. These changes in gait were present immediately after surgery, as well as 15 months later, when the animal had essentially recovered. Thus, control of the limbs in the horizontal plane was defective after loss of the low-frequency semicircular canal input and never recovered. Cycle-averaged pitch and roll head rotations, and 3-D head translations were also significantly larger and more erratic after than before surgery. Head rotations in yaw could not be quantified due to intrusion of voluntary head turns. These findings indicate that the semicircular canals provide critical low frequency information to maximize the accuracy of stepping and stabilize the head during normal quadrupedal locomotion.

Implications of gain modulation in brainstem circuits: VOR control system

Gain modulation is believed to be a common integration mechanism employed by neurons to combine information from various sources. Although gain fields have been shown to exist in some cortical and subcortical areas of the brain, their existence has not been explored in the brainstem. In the present modeling study, we develop a physiologically relevant simplified model for the angular vestibulo-ocular reflex (VOR) to show that gain modulation could also be the underlying mechanism that modifies VOR function with sensorimotor context (i.e. concurrent eye positions and stimulus intensity). The resulting nonlinear model is further extended to generate both slow and quick phases of the VOR. Through simulation of the hybrid nonlinear model we show that disconjugate eye movements during the VOR are an inevitable consequence of the existence of such gain fields in the bilateral VOR pathway. Finally, we will explore the properties of the predicted disconjugate component. We will demonstrate that the apparent phase characteristics of the disconjugate response vary with the concurrent conjugate component.

Effect of vestibular rehabilitation on passive dynamic visual acuity

While active dynamic visual acuity (DVA) has been shown to improve with gaze stabilization exercises, we sought to determine whether DVA during {passive} head impulses (pDVA) would also improve following a rehabilitation course of vestibular physical therapy (VPT) in patients with unilateral and bilateral vestibular hypofunction. VPT consisted of gaze and gait stabilization exercises done as a home exercise program. Scleral search coil was used to characterize the angular vestibulo-ocular reflex (aVOR) during pDVA before and after VPT. Mean duration of VPT was 66 ± 24 days, over a total of 5 ± 1.4 outpatient visits. Two of three subjects showed improvements in pDVA with a mean reduction of 43% (LogMAR 0.58 to 0.398 and 0.92 to 0.40). Our data suggest improvements in pDVA may be due in part to improvements in aVOR velocity and acceleration gains or reduced latency of the aVOR. Each subject demonstrated a reduction in the ratio of compensatory saccades to head impulses after VPT. Preliminary data suggest that active gaze stability exercises may contribute to improvements in pDVA in some individuals.

Endocochlear potential depends on Cl− channels: mechanism underlying deafness in Bartter syndrome IV

Human Bartter syndrome IV is an autosomal recessive disorder characterized by congenital deafness and severe renal salt and fluid loss. It is caused by mutations in BSND, which encodes barttin, a beta-subunit of ClC-Ka and ClC-Kb chloride channels. Inner-ear-specific disruption of Bsnd in mice now reveals that the positive potential, but not the high potassium concentration, of the scala media depends on the presence of these channels in the epithelium of the stria vascularis. The reduced driving force for K(+)-entry through mechanosensitive channels into sensory hair cells entails a profound congenital hearing loss and subtle vestibular symptoms. Although retaining all cell types and intact tight junctions, the thickness of the stria is reduced early on. Cochlear outer hair cells degenerate over several months. A collapse of endolymphatic space was seen when mice had additionally renal salt and fluid loss due to partial barttin deletion in the kidney. Bsnd(-/-) mice thus demonstrate a novel function of Cl(-) channels in generating the endocochlear potential and reveal the mechanism leading to deafness in human Bartter syndrome IV.

The Vestibulo-ocular Reflex During Active Head Motion in Chiari II Malformation

Chiari type II malformation (CII) is a developmental anomaly of the cerebellum and brainstem, which are important structures for processing the vestibulo-ocular reflex (VOR). We investigated the effects of the deformity of CII on the angular VOR during active head motion. Eye and head movements were recorded using an infrared eye tracker and magnetic head tracker in 20 participants with CII [11 males, age range 8-19 years, mean (SD) 14.4 (3.2) years]. Thirty-eight age-matched healthy children and adolescents (21 males) constituted the control group. Participants were instructed to 'look' in darkness at the position of their thumb, placed 25 cm away, while they made horizontal and vertical sinusoidal head rotations at frequencies of about 0.5 Hz and 2 Hz. Parametric and non-parametric tests were used to compare the two groups. The VOR gains, the ratio of eye to head velocities, were abnormally low in two participants with CII and abnormally high in one participant with CII. The majority of participants with CII had normal VOR performance in this investigation. However, the deformity of CII can impair the active angular VOR in some patients with CII. Low gain is attributed to brainstem damage and high gain to cerebellar dysfunction.

Incremental angular vestibulo-ocular reflex adaptation to active head rotation

Studies on motor learning typically present a constant adaptation stimulus, corresponding to the desired final adaptive state. Studies of the auditory and optokinetic systems provide compelling evidence that neural plasticity is enhanced when the error signal driving adaptation is instead adjusted gradually throughout training. We sought to determine whether the angular vestibulo-ocular reflex (aVOR) may be adaptively increased using an incremental velocity error signal (IVE) compared with a conventional constant and large velocity-gain demand (x2). We compared the magnitude of aVOR gain change for these two paradigms across different motion contexts (active and passive). Seven individuals with normal vestibular function and six individuals with unilateral vestibular hypofunction (UVH) were exposed to the IVE and x2 ("control") aVOR demand tasks. Each subject participated in 10 epochs of 30 active head impulses over a 15 min aVOR gain increase training session separately for the IVE and x2 paradigms, separated by either seven days (normal subjects) or 14 days (UVH subjects). For both normal and UVH subjects, both paradigms led to aVOR gain increase during the training session. For the normal subjects, the IVE paradigm led to larger aVOR gain change after training compared to the x2 paradigm, for both active (mean 17.3 +/- 4% vs. mean 7.1 +/- 9%, P = 0.029) and passive (mean 14.2 +/- 5% vs. 4.5 +/- 8%, P = 0.018) head impulses. For subjects with UVH, IVE produced a greater change in aVOR gain for active head impulses (mean 18.2 +/- 9.2% vs. mean -6 +/- 3.8%, P = 0.003). However, aVOR gains for passive head impulses were less consistent after IVE, with only two subjects displaying greater aVOR gain with this incremental paradigm. Some individuals generated compensatory saccades that occurred in the same direction of the deficient aVOR during either training paradigm. Our data suggest that the aVOR is modifiable when the velocity error signal is presented incrementally, and that this adaptation stimulus is particularly effective in the case of unilateral vestibular hypofunction. This has implications for programs of vestibular rehabilitation, where active head rotation is prescribed as a means to improve gaze stability.

The Effects of Cochlear Implantation on Vestibular Function

Objective 1) Measure vestibular function before and after cochlear implantation (CI) using a battery of tests covering the full range of stimulus frequencies over which the normal angular vestibulo-ocular reflex (VOR) stabilizes gaze. Methods Semicircular canal (SCC) function was assayed using head impulse test during 3-dimensional scleral search coil eye movement recordings (HIT), dynamic visual acuity during rapid head movements (DVA), head-shake nystagmus (HSN), and caloric electronystagmography (ENG). Saccular function was determined using vestibular-evoked myogenic potentials (VEMP). Patient self-assessment via the dizziness handicap inventory (DHI) and clinical head impulse testing (cHIT) were also measured. Results One of 28 post-implanted ears (4%) suffered severe loss of vestibular function in all 3 SCCs. HSN revealed no change in 11 subjects. ENG revealed new hypofunction in 1 of 16 ears (6%). Passive DVA revealed no significant change for 16 implanted ears. VEMP revealed significant increase or disappearance in threshold in 5 of 16 ears (31%). DHI scores were variable and correlated poorly with objective tests. The cHIT performed by one otolaryngologist in 14 subjects exhibited 44% sensitivity and 94% specificity for detection of severe hypofunction confirmed via quantitative HIT. Conclusions CI carries a small but nontrivial risk of iatrogenic vestibular hypofunction in the implanted ear. For bilateral simultaneous-CI, the risk of bilateral vestibular hypofunction is ∼0.16%, comparable to the likelihood of meningitis. The cHIT was highly specific for vestibular hypofunction in this study, but likely depends heavily on the examiner's threshold for abnormal.

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.

Head impulse test in unilateral vestibular loss

Quantitative head impulse test (HIT) measures the gain of the angular vestibulo-ocular reflex (VOR) during head rotation as the ratio of eye to head acceleration. Bedside HIT identifies subsequent catch-up saccades after the head rotation as indirect signs of VOR deficit. To determine the VOR deficit and catch-up saccade characteristics in unilateral vestibular disease in response to HIT of varying accelerations. Eye and head rotations were measured with search coils during manually applied horizontal HITs of varying accelerations in patients after vestibular neuritis (VN, n = 13) and unilateral vestibular deafferentation (UVD, n = 15) compared to normal subjects (n = 12). Normal VOR gain was close to unity and symmetric over the entire head-acceleration range. Patients with VN and UVD showed VOR gain asymmetry, with larger ipsilesional than contralesional deficits. As accelerations increased from 750 to 6,000 degrees /sec(2), ipsilesional gains decreased from 0.59 to 0.29 in VN and from 0.47 to 0.13 in UVD producing increasing asymmetry. Initial catch-up saccades can occur during or after head rotation. Covert saccades during head rotation are most likely imperceptible, while overt saccades after head rotation are detectable by clinicians. With increasing acceleration, the amplitude of overt saccades in patients became larger; however, initial covert saccades also became increasingly common, occurring in up to about 70% of trials. Head impulse test (HIT) with high acceleration reveals vestibulo-ocular reflex deficits better and elicits larger overt catch-up saccades in unilateral vestibular patients. Covert saccades during head rotation, however, occur more frequently with higher acceleration and may be missed by clinicians. To avoid false-negative results, bedside HIT should be repeated to improve chances of detection.

Why do patients with PSP fall?

Patients with progressive supranuclear palsy (PSP) fall frequently, beginning early in the course of their disease. Abnormal vestibulospinal reflexes are suspected, but the angular vestibulo-ocular reflex, which is mediated by the labyrinthine semicircular canals, survives late into the course of the disease. To test the hypothesis that otolithic-mediated reflexes are abnormal in PSP. We tested otolith-ocular reflexes (the translational vestibulo-ocular reflex [tVOR]) during combined rotation-translation in nine patients with PSP and nine age-matched control subjects; subjects viewed far and near targets. We also tested click-induced otolith-spinal reflexes (vestibular-evoked myogenic potentials [VEMPs]) in 10 patients with PSP and 30 age-matched controls. All patients with PSP had small tVOR responses during near viewing that were, on average, only 12% of those of control subjects (p = 0.001). Patients with PSP also showed a reduction of the amplitude of VEMPs compared to control subjects (median [range]: 54.3 [16.8 to 214] vs 149 [11.6 to 466], p = 0.001). Taken together, these results indicate that abnormal otolith-mediated reflexes may be at least partly responsible for frequent falls in progressive supranuclear palsy, and deserve further study.

Vergence-mediated modulation of the human angular vestibulo-ocular reflex is unaffected by canal plugging

The angular vestibulo-ocular reflex (AVOR) normally has an increased response during vergence on a near target. Some lines of evidence suggest that different vestibular afferent classes may contribute differentially to the vergence effect. For example, lesions that selectively affect those afferents sensitive to acceleration, i.e. irregular afferents, (galvanic ablation, intratympanic gentamicin) have been found to markedly reduce the vergence-mediated modulation of the AVOR. We hypothesized that a nonspecific and incomplete reduction in the AVOR response caused by canal plugging should have minimal effect on vergence-mediated modulation of the AVOR. The AVOR response to passive head impulses in canal planes (horizontal canals, left anterior-right posterior canals, right anterior-left posterior canals) while viewing a far (124 cm) or near (15 cm) target was measured in seven human subjects before and after anterior canal (AC) plugging to treat vertigo caused by dehiscence of the AC (i.e. superior canal dehiscence). The impulses were low amplitude (approximately 20 degrees ), high velocity ( approximately 150 degrees /s), high-acceleration (approximately 3,000 degrees /s(2)) head rotations administered manually by the investigator. Binocular eye and head velocity were recorded using the scleral search coil technique. The AVOR gain was defined as inverted eye velocity divided by head velocity. Before plugging, AVOR gain for the dehiscent AC went from 0.87 +/- 0.10 for far targets to 1.04 +/- 0.13 for near targets (+19.1 +/- 7.3%). After plugging, the AC AVOR gain went from 0.50 +/- 0.10 for far targets to 0.59 +/- 0.11 for near targets (+19.7 +/- 6.1%). There was no difference in the vergence-mediated gain increase between pre- and post-plugged conditions (multi-way analysis of variance: P = 0.66). AC plugging also did not change the latency of the AVOR for either AC. We hypothesize that canal plugging, unlike gentamicin or galvanic ablation, has no effect on vergence-mediated modulation of the AVOR because plugging does not preferentially affect irregular afferents.

Motorized head impulse rotator in patients with vestibular schwannoma

Conclusion. Motorized head impulse rotator is an effective technique to assess peripheral vestibular function. Approximately a quarter of patients with vestibular schwannoma (VS) had preserved preoperative responses. Vestibular disability could not be predicted based on vestibulo-ocular reflex (VOR) performance during motion stimuli, or in the caloric test. Objectives. To explore motorized head impulse rotator for evaluation of angular horizontal VOR in patients with VS, and to compare these responses to those of the caloric test and the symptoms. Patients and methods. We prospectively recorded head and eye position during unpredictable motorized head impulses in 38 patients with VS. We calculated gain and asymmetry of VOR (mean±95% CI), and the results were compared to those of the caloric test and a questionnaire regarding dizziness, hearing and quality of life. Results. The VOR during motorized impulses was abnormal in 71% of patients. Asymmetry in gain correlated significantly (p<0.001) with unilateral weakness in the caloric test. Preoperative gain was significantly lowered to 0.83±0.08 on the ipsilateral side compared to 0.98±0.06 on the contralateral side. Postoperative gain on the operated side of 0.53±0.05 was significantly different from preoperative gain (p<0.001). Findings in vestibular tests did not correlate with subjective sensation of dizziness.

Vestibulo-ocular responses to vertical translation in normal human subjects

Prior studies of the human translational vestibulo-ocular reflex (tVOR) report that eye rotations amount to less than 60% of those required to keep the eyes pointed at a stationary visual target, unlike the angular VOR (aVOR) which is optimized to maintain stable gaze. Our first goal was to determine if the performance of the tVOR improves when head translations are combined with head rotations in ambient lighting. A second goal was to measure tVOR during vertical head translations (bob), which has not received systematic study. We measured tVOR alone and in combination with the aVOR in 20 normal human subjects, aged 25-72 years, as they sat on a moving platform that bobbed at 2.0 Hz while rotating horizontally (yaw) at 1.0 Hz. When subjects viewed a visual target at 2 m, median "compensation gain" (eye rotational velocity/required eye rotational velocity to maintain foveal target fixation) was 0.52 during pure bob and 0.59 during combined bob-yaw; during viewing of a near target at approximately 17 cm, compensation gain was 0.58 for pure bob and 0.60 for combined bob-yaw. Mean phase lag of eye-in-head velocity for the tVOR was approximately 19 degrees with respect to the ideal compensatory response, irrespective of whether translation was accompanied by rotation. Thus, the tVOR changed only slightly during translation-rotation versus pure translation, and our subjects' ocular rotations remained at about 60% of those required to point the eyes at the target. Comparison of response during binocular or monocular viewing, and ambient or reduced illumination, indicated that relative image motion between the target and background was an important determinant of tVOR behavior. We postulate that tVOR evolved not to stabilize the image of the target on the fovea, but rather to minimize retinal image motion between objects lying in different planes, in order to optimize motion parallax information.

The vestibulo-ocular reflex during active head motion in children and adolescents

Little information is available on the performance and maturity of the vestibulo-ocular reflex (VOR) in children and adolescents during active head motion as encountered during normal locomotion. We investigated the active VOR performance in children and adolescents to determine its norm and variation with age. We recorded the angular active VOR using an infrared eye tracker and a magnetic head tracker in 38 children, aged 8-19 years. Participants made sinusoidal head-on-body rotations in yaw (left-right) and pitch (up-down) at frequencies of about 0.5 and 2 Hz in the dark. Mean VOR gains, the ratios of eye to head velocities, were close to unity and were significantly higher at 2 Hz than at 0.5 Hz. VOR gains did not vary with age. The angular VOR during active head motion is functionally mature in children 8 years or older at 0.5 and 2 Hz head rotations.

Modification of compensatory saccades after aVOR gain recovery

The recruitment of extra-vestibular mechanisms to assist a deficient angular vestibulo-ocular reflex (aVOR) during ipsilesional head rotations is well established and includes saccades of reduced latency that occur in the direction of the lesioned aVOR, termed compensatory saccades (CS). Less well known is the functional relevance of these unique saccades. Here we report a 42 y.o. male diagnosed with right unilateral vestibular hypofunction due to vestibular neuronitis who underwent a vestibular rehabilitation program including gaze stabilization exercises. After three weeks, he had a significant improvement in his ability to see clearly during head rotation. Our data show a reduction in the recruitment and magnitude of CS as well as improved peripheral aVOR gain (eye velocity/head velocity) and retinal eye velocity. Our data suggest an inverse, dynamic relationship between the recruitment of CS and the gain of the aVOR.

A Multichannel Semicircular Canal Neural Prosthesis Using Electrical Stimulation to Restore 3-D Vestibular Sensation

Bilateral loss of vestibular sensation can be disabling. Those afflicted suffer illusory visual field movement during head movements, chronic disequilibrium and postural instability due to failure of vestibulo-ocular and vestibulo-spinal reflexes. A neural prosthesis that emulates the normal transduction of head rotation by semicircular canals could significantly improve quality of life for these patients. Like the three semicircular canals in a normal ear, such a device should at least transduce three orthogonal (or linearly separable) components of head rotation into activity on corresponding ampullary branches of the vestibular nerve. We describe the design, circuit performance and in vivo application of a head-mounted, semi-implantable multichannel vestibular prosthesis that encodes head movement in three dimensions as pulse-frequency-modulated electrical stimulation of three or more ampullary nerves. In chinchillas treated with intratympanic gentamicin to ablate vestibular sensation bilaterally, prosthetic stimuli elicited a partly compensatory angular vestibulo-ocular reflex in multiple planes. Minimizing misalignment between the axis of eye and head rotation, apparently caused by current spread beyond each electrode's targeted nerve branch, emerged as a key challenge. Increasing stimulation selectivity via improvements in electrode design, surgical technique and stimulus protocol will likely be required to restore AVOR function over the full range of normal behavior.

Semicircular Canal Function Before and After Surgery for Superior Canal Dehiscence

To characterize semicircular canal function before and after surgery for superior semicircular canal dehiscence (SCD) syndrome. Prospective unblinded study of physiologic effect of intervention. Tertiary referral center. Patients with SCD syndrome documented by history, sound- or pressure-evoked eye movements, vestibular-evoked myogenic potential testing, and high-resolution multiplanar computed tomographic scans. Nineteen subjects with SCD had quantitative measurements of their angular vestibulo-ocular reflexes (AVOR) in response to rapid rotary head thrusts measured by magnetic search coil technique before and after middle fossa approach and repair of the dehiscence. In 18 subjects, the dehiscence was plugged; and in 1, it was resurfaced. The AVOR gains (eye velocity/head velocity) for excitation of each of the semicircular canals. Vertigo resulting from pressure or loud sounds resolved in each case. Before surgery, mean AVOR gains were normal for the ipsilateral horizontal (0.94 +/- 0.07) and posterior (0.84 +/- 0.09) canals. For the superior canal to be operated on, AVOR gain was 0.75 +/- 0.13; but this was not significantly lower than the gain for the contralateral superior canal (0.82 +/- 0.11, p = 0.08). Mean AVOR gain decreased by 44% for the operated superior canals (to 0.42 +/- 0.11, p < 0.0001). There was a 13% decrease in gain for the ipsilateral posterior canal (p = 0.02), perhaps because plugging affected the common crus in some cases. There was a 10% decrease in gain for excitation of the contralateral posterior canal (p < 0.0001), which likely reflects the loss of the inhibitory contribution of the plugged superior canal during head thrusts exciting the contralateral posterior canal. Mean AVOR gain did not change for any of the other canals, but two subjects did develop hypofunction of all three ipsilateral canals postoperatively. Middle fossa craniotomy and repair of SCD reduce the function of the operated superior canal but typically preserve the function of the other ipsilateral semicircular canals.

Motorized Head Impulse Rotator for Horizontal Vestibulo-ocular Reflex

To characterize the horizontal angular vestibulo-ocular reflex using a new motorized head impulse rotator and electro-oculography technique. Prospective case-control study. We included 22 healthy volunteers with unpredictable, horizontal motorized head impulses with a mean velocity of 170 degrees/s and a mean acceleration of 1550 degrees/s2. We recorded head and eye position and calculated gain, asymmetry, and latency of the vestibulo-ocular reflex. All subjects underwent testing twice while viewing a far (140 cm) target to evaluate the repeatability of the measurement. In addition, 8 of these subjects underwent testing while viewing a near (15 cm) target. We reported findings as mean +/- SD. The mean gain during the 30-millisecond interval before peak head velocity and during the interval when head velocity ranged from 100 degrees /s to 120 degrees/s was 1.08 +/- 0.10. The mean asymmetry in gain between sides was 3.7% +/- 2.8%, and the mean latency of the vestibulo-ocular reflex was 3.4 +/- 6.3 milliseconds. There was a statistically significant correlation between consecutive gain measurements for each subject (r = 0.59; P=.004). The mean gain for the near target was 1.26 +/- 0.10 and was significantly higher than that for the far target (P = .002). The vestibulo-ocular reflex measurements using our novel system are comparable to those achieved using other techniques. These results suggest that a motorized head impulse rotator with electro-oculography allows reliable and fast measurement of the vestibulo-ocular reflex. In addition, the method is safe, repeatable, and thus could be a useful tool in the clinical assessment of the vestibulo-ocular reflex.