Slow-phase Eye Research Articles

The video head impulse test during post-rotatory nystagmus: physiology and clinical implications

The aim of this study was to test the effects of a sustained nystagmus on the head impulse response of the vestibulo-ocular reflex (VOR) in healthy subjects. VOR gain (slow-phase eye velocity/head velocity) was measured using video head impulse test goggles. Acting as a surrogate for a spontaneous nystagmus (SN), a post-rotatory nystagmus (PRN) was elicited after a sustained, constant-velocity rotation, and then head impulses were applied. 'Raw' VOR gain, uncorrected for PRN, in healthy subjects in response to head impulses with peak velocities in the range of 150°/s-250°/s was significantly increased (as reflected in an increase in the slope of the gain versus head velocity relationship) after inducing PRN with slow phases of nystagmus of high intensity (>30°/s) in the same but not in the opposite direction as the slow-phase response induced by the head impulses. The values of VOR gain themselves, however, remained in the normal range with slow-phase velocities of PRN < 30°/s. Finally, quick phases of PRN were suppressed during the first 20-160 ms of a head impulse; the time frame of suppression depended on the direction of PRN but not on the duration of the head impulse. Our results in normal subjects suggest that VOR gains measured using head impulses may have to be corrected for any superimposed SN when the slow-phase velocity of nystagmus is relatively high and the peak velocity of the head movements is relatively low. The suppression of quick phases during head impulses may help to improve steady fixation during rapid head movements.

Preserved otolith organ function in caspase-3-deficient mice with impaired horizontal semicircular canal function.

Genetically engineered mice are valuable models for elucidation of auditory and vestibular pathology. Our goal was to establish a comprehensive vestibular function testing system in mice using: (1) horizontal angular vestibulo-ocular reflex (hVOR) to evaluate semicircular canal function and (2) otolith-ocular reflex (OOR) to evaluate otolith organ function and to validate the system by characterizing mice with vestibular dysfunction. We used pseudo off-vertical axis rotation to induce an otolith-only stimulus using a custom-made centrifuge. For the OOR, horizontal slow-phase eye velocity and vertical eye position were evaluated as a function of acceleration. Using this system, we characterized hVOR and OOR in the caspase-3 (Casp3) mutant mice. Casp3 (-/-) mice had severely impaired hVOR gain, while Casp3 (+/-) mice had an intermediate response compared to WT mice. Evaluation of OOR revealed that at low-to-mid frequencies and stimulus intensity, Casp3 mutants and WT mice had similar responses. At higher frequencies and stimulus intensity, the Casp3 mutants displayed mildly reduced otolith organ-related responses. These findings suggest that the Casp3 gene is important for the proper function of the semicircular canals but less important for the otolith organ function.

Positive or Negative Feedback of Optokinetic Signals: Degree of the Misrouted Optic Flow Determines System Dynamics of Human Ocular Motor Behavior

The optokinetic system in healthy humans is a negative-feedback system that stabilizes gaze: slow-phase eye movements (i.e., the output signal) minimize retinal slip (i.e., the error signal). A positive-feedback optokinetic system may exist due to the misrouting of optic fibers. Previous studies have shown that, in a zebrafish mutant with a high degree of the misrouting, the optokinetic response (OKR) is reversed. As a result, slow-phase eye movements amplify retinal slip, forming a positive-feedback optokinetic loop. The positive-feedback optokinetic system cannot stabilize gaze, thus leading to spontaneous eye oscillations (SEOs). Because the misrouting in human patients (e.g., with a condition of albinism or achiasmia) is partial, both positive- and negative-feedback loops co-exist. How this co-existence affects human ocular motor behavior remains unclear. We presented a visual environment consisting of two stimuli in different parts of the visual field to healthy subjects. One mimicked positive-feedback optokinetic signals and the other preserved negative-feedback optokinetic signals. By changing the ratio and position of the visual field of these visual stimuli, various optic nerve misrouting patterns were simulated. Eye-movement responses to stationary and moving stimuli were measured and compared with computer simulations. The SEOs were correlated with the magnitude of the virtual positive-feedback optokinetic effect. We found a correlation among the simulated misrouting, the corresponding OKR, and the SEOs in humans. The proportion of the simulated misrouting needed to be greater than 50% to reverse the OKR and at least greater than or equal to 70% to evoke SEOs. Once the SEOs were evoked, the magnitude positively correlated to the strength of the positive-feedback OKR. This study provides a mechanism of how the misrouting of optic fibers in humans could lead to SEOs, offering a possible explanation for a subtype of infantile nystagmus syndrome (INS).

Magnetic Vestibular Stimulation in Subjects with Unilateral Labyrinthine Disorders

We recently discovered that static magnetic fields from high-strength MRI machines induce nystagmus in all normal humans, and that a magneto-hydrodynamic Lorentz force, derived from ionic currents in the endolymph and pushing on the cupula, best explains this effect. Individuals with no labyrinthine function have no nystagmus. The influence of magnetic vestibular stimulation (MVS) in individuals with unilateral deficits in labyrinthine function is unknown and may provide insight into the mechanism of MVS. These individuals should experience MVS, but with a different pattern of nystagmus consistent with their unilateral deficit in labyrinthine function. We recorded eye movements in the static magnetic field of a 7 T MRI machine in nine individuals with unilateral labyrinthine hypofunction, as determined by head impulse testing and vestibular-evoked myogenic potentials (VEMP). Eye movements were recorded using infrared video-oculography. Static head positions were varied in pitch with the body supine, and slow-phase eye velocity (SPV) was assessed. All subjects exhibited predominantly horizontal nystagmus after entering the magnet head-first, lying supine. The SPV direction reversed when entering feet-first. Pitching chin-to-chest caused subjects to reach a null point for horizontal SPV. Right unilateral vestibular hypofunction (UVH) subjects developed slow-phase-up nystagmus and left UVH subjects, slow-phase-down nystagmus. Vertical and torsional components were consistent with superior semicircular canal excitation or inhibition, respectively, of the intact ear. These findings provide compelling support for the hypothesis that MVS is a result of a Lorentz force and suggest that the function of individual structures within the labyrinth can be assessed with MVS. As a novel method of comfortable and sustained labyrinthine stimulation, MVS can provide new insights into vestibular physiology and pathophysiology.

Velocity storage mechanism in zebrafish larvae

The optokinetic reflex (OKR) and the angular vestibulo-ocular reflex (aVOR) complement each other to stabilize images on the retina despite self- or world motion, a joint mechanism that is critical for effective vision. It is currently hypothesized that signals from both systems integrate, in a mathematical sense, in a network of neurons operating as a velocity storage mechanism (VSM). When exposed to a rotating visual surround, subjects display the OKR, slow following eye movements frequently interrupted by fast resetting eye movements. Subsequent to light-off during optokinetic stimulation, eye movements do not stop abruptly, but decay slowly, a phenomenon referred to as the optokinetic after-response (OKAR). The OKAR is most likely generated by the VSM. In this study, we observed the OKAR in developing larval zebrafish before the horizontal aVOR emerged. Our results suggest that the VSM develops prior to and without the need for a functional aVOR. It may be critical to ocular motor control in early development as it increases the efficiency of the OKR.

A randomised double-blind, cross-over trial of 4-aminopyridine for downbeat nystagmus—effects on slowphase eye velocity, postural stability, locomotion and symptoms

ObjectiveThe effects of 4-aminopyridine (4-AP) on downbeat nystagmus (DBN) were analysed in terms of slow-phase velocity (SPV), stance, locomotion, visual acuity (VA), patient satisfaction and side effects using standardised questionnaires.MethodsTwenty-seven...

Contributions of retinal direction‐selective ganglion cells to optokinetic responses in mice

In the mouse retina, there are two distinct groups of direction-selective ganglion cells, ON and ON-OFF, that detect movement of visual images. To understand the roles of these cells in controlling eye movements, we studied the optokinetic responses (OKRs) of mutant mice with dysfunctional ON-bipolar cells that have a functional obstruction of transmission to ON direction-selective ganglion cells. Experiments were carried out to examine the initial and late phases of OKRs. The initial phase was examined by measurement of eye velocity using stimuli of sinusoidal grating patterns of various spatiotemporal frequencies that moved for 0.5s. The mutant mice showed significant initial OKRs, although the range of spatiotemporal frequencies that elicited these OKRs was limited and the response magnitude was weaker than that in wild-type mice. To examine the late phase of the OKRs, the same visual patterns were moved for 30s to induce alternating slow and quick eye movements (optokinetic nystagmus) and the slow-phase eye velocity was measured. Wild-type mice showed significant late OKRs with a stimulus in an appropriate range of spatiotemporal frequencies (0.0625-0.25cycles/°, 0.75-3.0Hz, 3-48°/s), but mutant mice did not show late OKRs in response to the same visual stimuli. The results suggest that two groups of direction-selective ganglion cells play different roles in OKRs: ON direction-selective ganglion cells contribute to both initial and late OKRs, whereas ON-OFF direction-selective ganglion cells contribute to OKRs only transiently.

Glycine Receptor Deficiency and Its Effect on the Horizontal Vestibulo-ocular Reflex: a Study on the SPD1J Mouse

Inhibition is critical in the pathways controlling the vestibulo-ocular reflex (VOR) and plays a central role in the precision, accuracy and speed of this important vestibular-mediated compensatory eye movement. While γ-aminobutyric acid is the common fast inhibitory neurotransmitter in most of the VOR microcircuits, glycine is also found in key elements. For example, the omnidirectional pause neurons (OPNs) and inhibitory burst neurons in the horizontal VOR both use glycine as their preferred inhibitory neurotransmitter. Determining the precise contribution of glycine to the VOR pathway has been difficult due to the lack of selective tools; however, we used spasmodic mice that have a naturally occurring defect in the glycine receptor (GlyR) that reduces glycinergic transmission. Using this animal model, we compared the horizontal VOR in affected animals with unaffected controls. Our data showed that initial latency and initial peak velocity as well as slow-phase eye movements were unaffected by reduced glycinergic transmission. Importantly however, there were significant effects on quick-phase activity, substantially reducing their number (30-70 %), amplitude (~55 %) and peak velocity (~38 %). We suggest that the OPNs were primarily responsible for the reduced quick-phase properties, since they are part of an unmodifiable, or more 'hard-wired', microcircuit. In contrast, the effects of reduced glycinergic transmission on slow-phases were likely ameliorated by the intrinsically modifiable nature of this pathway. Our results also suggested there is a 'threshold' in GlyR-affected animals, below which the effects of reduced glycinergic transmission were undetected.

Transmastoid galvanic stimulation does not affect the vergence-mediated gain increase of the human angular vestibulo-ocular reflex

Vergence is one of several viewing contexts that require an increase in the angular vestibular-ocular reflex (aVOR) response. A previous monkey study found that the vergence-mediated gain (eye/head velocity) increase of the aVOR was attenuated by 64% when anodic currents, which preferentially lower the activity of irregularly firing vestibular afferents, were delivered to both labyrinths. We sought to determine whether there was similar evidence implicating a role for irregular afferents in the vergence-mediated gain increase of the human aVOR. Our study is based upon analysis of the aVOR evoked by head rotations, delivered passively while subjects viewed a near (15cm) or far (124cm) target and applying galvanic vestibular stimulation (GVS) via surface electrodes. We tested 12 subjects during 2-3 sessions each. Vestibular stimuli consisted of passive whole-body rotations (sinusoids from 0.05-3Hz and 12-25°/s, and transients with peak ~15°, 50°/s, 500°/s(2)) and head-on-body impulses (peak ~30°, 150°/s, 3,000°/s(2)). GVS was on for 10s every 20s. All polarity combinations were tested, with emphasis on uni- and bi-lateral anodic inhibition. The average stimulus current was 5.9±1.6mA (range: 3-9.5mA), vergence angle (during near viewing) was 22.6±2.8° and slow-phase eye velocity caused by left anodic current stimulation with head stationary was -3.4±1.1°/s, -0.2±0.6°/s and 2.5±1.4°/s (torsion, vertical, horizontal). No statistically significant GVS effects were observed, suggesting that surface electrode GVS has no effect on the vergence-mediated gain increase of the aVOR at the current levels (~6mA) tolerated by most humans. We conclude that clinically practical transmastoid GVS does not effectively silence irregular afferents and hypothesize that currents >10mA are needed to reproduce the monkey results.

A dynamic model for eye‐position‐dependence of spontaneous nystagmus in acute unilateral vestibular deficit (Alexander's Law)

Spontaneous nystagmus (SN) is a symptom of acute vestibular tone asymmetry. Alexander's Law (AL) states that slow-phase velocity of SN is higher when looking in the direction of fast-phases of nystagmus and lower in the slow-phase direction. Earlier explanations for AL predict that during SN, slow-phase eye velocity is a linear function of eye position, increasing linearly as eye deviates towards the fast-phase direction. Recent observations, however, show that this is often not the case; eye velocity does not vary linearly with eye position. Such new findings necessitate a re-evaluation of our understanding of AL. As AL may be an adaptive response of the vestibular system to peripheral lesions, understanding its mechanism could shed light on early adaptation strategies of the brain. Here, we propose a physiologically plausible mechanism for AL that explains recent experimental data. We use a dynamic control system model to simulate this mechanism and make testable predictions. This mechanism is based on the known effects of unilateral vestibular deficit on the response of the ipsi- and contralesional vestibular nuclei (VN) of the brainstem. This hypothesis is based on the silencing of the majority of ipsilesional VN units, which creates an asymmetry between the responses of the ipsi- and contralesional VN. Unlike former explanations, the new hypothesis does not rely on lesion detection strategies or signals originating in higher brain structures. The proposed model demonstrates possible consequences of acute peripheral deficits for the function of the velocity-to-position neural integrator of the ocular motor system and the vestibulo-ocular reflex.

Comprehensive Analysis of Head-Shaking Nystagmus in Patients with Vestibular Neuritis

Although biphasic head-shaking nystagmus (HSN) is a basic response to head shaking in patients with unilateral vestibular loss, monophasic HSN is commonly seen in patients with dizziness of undetermined etiology. Since the clinical significance of HSN remains unclear, we sought to characterize different types of HSN in patients with vestibular neuritis (VN) during the acute stage (within 7 days after the onset of vertigo) and at follow-up (about 2 months after the onset of vertigo), and to compare HSN and caloric responses. We analyzed HSN, spontaneous nystagmus and caloric tests in 66 patients with VN. Overall, HSN showed high abnormal rates (94 and 89%) during the acute and follow-up stages and could detect vestibular hypofunction even when canal paresis (CP) had normalized at follow-up. All patients in the acute stage and most patients at follow-up showed HSN with the slow phase to the lesioned side (paretic). Biphasic HSN was common at follow-up, and many patients with a monophasic paretic pattern during the acute stage had evolved to a biphasic paretic pattern at follow-up. Initial slow-phase eye velocities (SPVs) in biphasic HSN were larger than those in monophasic HSN at follow-up. Absence of HSN or reversal of its direction was closely related to normalized caloric responses, but SPVs of HSN did not correlate with the severity of CP. These findings indicate that the HSN test is a sensitive detector of vestibular hypofunction upon 2-Hz head rotation. HSN may reveal previous vestibular hypofunction in the 2-Hz frequency range even at follow-up, when caloric responses detecting vestibular hypofunction in the low-frequency range had normalized. The two tests utilize different mechanisms to assess vestibular hypofunction and are complementary. Biphasic paretic HSN is the most common pattern at follow-up and occurs when the initial SPVs induced by head rotation are large enough to induce the adaptation of primary vestibular afferent activity. Monophasic HSN, which is commonly found in dizzy patients, indicates less severe vestibular hypofunction than biphasic HSN in the 2-Hz frequency range, and the caloric tests can provide further information about the side and presence of vestibular hypofunction at lower frequencies.

Interaction between vestibulo-spinal and corticospinal systems: a combined caloric and transcranial magnetic stimulation study

We investigated the interaction between vestibular and corticospinal stimuli in 8 healthy volunteers. Vestibular stimulation was induced with unilateral ear caloric irrigation (30°C) with subjects supine. Single transcranial magnetic stimulation (TMS) pulses were delivered (double-cone coil, intensities 60-75% maximal output) every 10-20s during vestibular activation and during baseline. Bilateral surface electromyography (EMG) from splenius capitis, sternocleidomastoid (SCM), obliquus externus abdominis, vastus lateralis, biceps femoris (BF), tibialis anterior and peroneus longus was obtained. During whole-body maximal rotatory voluntary isometric contraction (MRVC), only SCM and BF displayed EMG activation/inhibition patterns indicating axial rotatory action. TMS-induced motor evoked potentials (MEPs) after caloric irrigation revealed that only SCM showed consistent vestibular-mediated excitation/inhibition responses, i.e. an increase in MEP area contralateral to the irrigation and a decrease in MEP area ipsilaterally (+12.7 and -6.3% of the MRVC, respectively). A putative head turn induced by this SCM activity pattern would be in the same direction of the slow-phase eye movement. EMG in the 100ms preceding TMS showed muscle tone values of approximately 10% of MRVC. After caloric irrigation, these values increased by ca. 2% for all muscles bilaterally and hence cannot explain the direction-specific SCM MEP changes. Thus, SCM MEPs show caloric-induced amplitude modulation indicating that SCM is under both horizontal semicircular canal and corticospinal control. This vestibular modulation of corticospinal SCM control likely occurs at cortical levels. The direction of the MEP modulation indicates a directional coupling between vestibularly induced head and eye movements.

Relationship of slow-phase velocity to visual acuity in infantile nystagmus associated with albinism

To investigate the relationship between slow-phase velocity of nystagmus and visual acuity in children with albinism. Twelve children with infantile nystagmus associated with albinism had eye movements recorded by binocular video-oculography (10 patients) or by scleral search coil (2 patients). In children younger than 3 years of age visual acuities was assessed by means of Teller acuity cards and corrected for age. Histograms of horizontal eye velocities were fit by a gamma distribution in all patients (r2>0.85). The velocity at the peak of the gamma distribution was compared with the limiting velocity predicted by the dynamic visual acuity (DVA) model. All histograms of slow-phase eye velocity were skewed toward lower velocities, with the peak distribution ranging from 5 to 20 degrees/second. The velocity at the peak of the gamma distribution for each subject was uniformly equal to or below the limiting velocity predicted by the DVA model. The average of the gamma distribution across all subjects corresponded to an upper limit to eye velocity of 17 degrees/second. At this velocity the DVA model predicted visual acuity of 20/50, which is lower than the average visual acuity reported in albinism. The distributions of eye velocity were lower than the limiting eye velocity predicted on the basis of DVA almost 50% of the time. Visual acuity in albinism is limited by macular hypoplasia rather than by slow-phase eye velocity of nystagmus.

Characterization of the Electrically Evoked Compound Action Potential of the Vestibular Nerve

We recorded intraoperative and postoperative electrically evoked compound action potentials (ECAPs) in rhesus monkeys implanted with a vestibular neurostimulator. The objectives were to correlate the generation of slow-phase nystagmus or eye twitches induced by electrical stimulation of the implanted semicircular canal with the presence or absence of the vestibular ECAP responses and to assess the effectiveness of ECAP monitoring during surgery to guide surgical insertion of electrode arrays into the canals. Four rhesus monkeys (a total of 7 canals) were implanted with a vestibular neurostimulator modified from the Nucleus Freedom cochlear implant. ECAP recordings were obtained during surgery or at various intervals after surgery using the Neural Response Telemetry feature of the clinical Custom Sound EP software. Eye movements during electrical stimulation of individual canals were recorded with a scleral search coil system in the same animals. Measurable vestibular ECAPs were observed intraoperatively or postoperatively in 3 implanted animals. Robust and sustained ECAPs were obtained in 3 monkeys at the test intervals of 0, 7, or greater than 100 days after implantation surgery. In all 3 animals, stimulation with electrical pulse trains produced measurable eye movements in a direction consistent with the vestibulo-ocular reflex from the implanted semicircular canal. In contrast, electrically evoked eye movements could not be measured in 3 of the 7 implanted canals, none of which produced distinct vestibular ECAPs. In 2 animals, ECAP waveforms were systematically monitored during surgery, and the procedure proved crucial to the success of vestibular implantation. Vestibular ECAPs exhibit similar morphology and growth characteristics to cochlear ECAPs from human cochlear implant patients. The ECAP measure is well correlated with the functional activation of eye movements by electrical stimulation after implantation surgery. The intraoperative ECAP recording technique is an efficient tool to guide the placement of electrode array into the semicircular canals.

Test-retest reliability of vibration-induced nystagmus in peripheral dizzy patients

The purpose of this study was to analyze test-retest reliability of vibration-induced nystagmus (VIN) in dizzy patients. Fifty-two consecutive patients with positive eye movements induced by vibration at all four different stimulation sites were enrolled. Evaluation of VIN was repeated in 2 separate sessions, 30 minutes apart. Maximum slow-phase eye velocities at different sites from the first and second sessions were assessed via the intraclass correlation coefficient (ICC) and the Pearson correlation coefficient. The incidence of directional changing of evoked nystagmus and the abnormal rates were also evaluated. Excellent reliability with ICC values ranging from 0.89-0.98 and substantial-to-excellent correlation was obtained for the maximum slow-phase eye velocities at different sites. The incidence of directional changes of evoked nystagmus was 0%-4% at each stimulation site. Forty-three patients (83%) had abnormal results in the first session and 41 patients (79%) had abnormal results in the second session. Overall, the direction and maximum slow-phase eye velocities of VIN for different stimulation sites had excellent test-retest reliability. The VIN test is a reliable test for detecting vestibular imbalance in evaluating a dizzy patient.

Velocity Storage Contribution to Vestibular Self-Motion Perception in Healthy Human Subjects

Self-motion perception after a sudden stop from a sustained rotation in darkness lasts approximately as long as reflexive eye movements. We hypothesized that, after an angular velocity step, self-motion perception and reflexive eye movements are driven by the same vestibular pathways. In 16 healthy subjects (25-71 years of age), perceived rotational velocity (PRV) and the vestibulo-ocular reflex (rVOR) after sudden decelerations (90°/s(2)) from constant-velocity (90°/s) earth-vertical axis rotations were simultaneously measured (PRV reported by hand-lever turning; rVOR recorded by search coils). Subjects were upright (yaw) or 90° left-ear-down (pitch). After both yaw and pitch decelerations, PRV rose rapidly and showed a plateau before decaying. In contrast, slow-phase eye velocity (SPV) decayed immediately after the initial increase. SPV and PRV were fitted with the sum of two exponentials: one time constant accounting for the semicircular canal (SCC) dynamics and one time constant accounting for a central process, known as velocity storage mechanism (VSM). Parameters were constrained by requiring equal SCC time constant and VSM time constant for SPV and PRV. The gains weighting the two exponential functions were free to change. SPV were accurately fitted (variance-accounted-for: 0.85 ± 0.10) and PRV (variance-accounted-for: 0.86 ± 0.07), showing that SPV and PRV curve differences can be explained by a greater relative weight of VSM in PRV compared with SPV (twofold for yaw, threefold for pitch). These results support our hypothesis that self-motion perception after angular velocity steps is be driven by the same central vestibular processes as reflexive eye movements and that no additional mechanisms are required to explain the perceptual dynamics.

Hyperventilation-Induced Nystagmus in Patients with Vestibular Neuritis in the Acute and Follow-Up Stages

Objective: Our purposes were to characterize hyperventilation-induced nystagmus (HVIN) in patients with unilateral vestibular neuritis (VN) through follow-up examinations and to determine the effects of hyperventilation on vestibular imbalance in patients with VN. Materials and Methods: The horizontal eye movements in 35 patients with acute VN were recorded. The eye movements were analyzed and the maximum value of slow-phase eye velocity (SPV) was obtained during and after hyperventilation. Nineteen of 35 patients underwent follow-up examinations around 7 weeks later. When spontaneous nystagmus was present, the SPV of spontaneous nystagmus was subtracted from that of HVIN. A maximum SPV of HVIN of ≧4°/s was considered abnormal. The direction and SPV of HVIN were analyzed. Results: The incidence of HVIN in patients with VN was significantly higher in the acute stage (18 of 35; 51%) than the follow-up stage (4 of 19; 21%). The direction of HVIN present in the follow-up stage was entirely towards the contralesional side (contralesional HVIN). However, the direction of HVIN in the acute stage was mixed, towards the contralesional side (10 of 35; 28%) and towards the ipsilesional side (8 of 35; 23%). The SPVs (49 ± 56°/s) of ipsilesional HVIN were significantly greater than the contralesional HVIN in the acute stage (8 ± 3°/s). Robust nystagmus (SPV ≧25°/s) was entirely ipsilesional HVIN, which was observed only in the acute stage. Conclusions: Our findings indicate that hyperventilation can result in aggravation of vestibular imbalance in the acute and follow-up stages in different ways. Hyperventilation resulted in contralesional HVIN in both the acute and follow-up stages, each in approximately a fourth of the patients, which suggests a disruption of central static compensatory mechanisms. However, ipsilesional HVIN was elicited only in the acute stage (in approximately a fourth of the patients). About half of the patients with ipsilesional HVIN showed robust responses, which is a characteristic finding, suggesting a transient intense increase in vestibular activity on the lesional side.

Eccentric gaze dynamics enhance vection in depth

This study examined the role of eccentric gaze dynamics in the generation of visual illusions of self-motion (i.e., vection). In Experiment 1, observers maintained their gaze either upward, downward, leftward, or rightward with respect to the center of a radially expanding optic flow pattern, which simulated forward self-motion in depth through a 3D cloud of objects. Real-time vection strength ratings and changes in horizontal and vertical eye positions were recorded simultaneously. Vection strength was found to increase progressively over the course of each 30-s presentation of radial flow. Eye tracking revealed strong optokinetic responses, consistent with ocular following responses (OFRs). Reported increases in vection strength in all four gaze conditions were typically preceded by reductions in slow-phase eye velocity. Similar results were found in Experiment 2, where displays simulated self-motion over a ground plane, which provided superior perspective. We conclude in both cases that enhancements of vection strength over time were temporally contingent upon the changing character of OFR while viewing these displays.

Rotational Tests of Vestibular Function

Rotational tests are aimed at producing a more natural, precise, repeatable, and broadband evaluation of the vestibular function. Currently, two types of rotation tests are in clinical use: passive whole-body rotation where the stimulus is produced by a motorized chair, and active rotation where the stimulus is produced by voluntary head movements. In both methods, the frequency response of the vestibulo-ocular reflex (VOR) is determined by measuring the eye movements and comparing the head velocity with the slow-phase eye velocity. Rotation tests offer several advantages over other vestibular function tests in patients with bilateral caloric weakness, in young children, or in patients for whom VOR changes have to be assessed over time. In most other patients, rotation tests do not offer a significant advantage because of their low sensitivity to common vestibular abnormalities.

On‐Line Classification and Prediction of Eye Movements by Multiple‐Model Kalman Filtering

An extensible multiple-model Kalman filter framework for eye tracking and video-oculography (VOG) applications is proposed. The Kalman filter predicts future states of a system on the basis of a mathematical model and previous measurements. The predicted values are then compared against the current measurements. In a correcting step, the predicted state is enhanced by the measurements. In this work, the Kalman filter is used for smoothing the VOG data, for on-line classification of eye movements, as well as for predictive real-time control of a gaze-driven head-mounted camera (EyeSeeCam). With multiple models running in parallel, it was possible to distinguish between fixations, slow-phase eye movements, and saccades. Under the assumption that each class of eye movement follows a distinct model, one can decide which types of eye movement occurred by evaluating the probability for each model.