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Postural instability is a common symptom of vestibular dysfunction that impacts a person’s day-to-day activities. Vestibular rehabilitation is effective in decreasing dizziness, visual symptoms and improving postural control through several mechanisms including sensory reweighting of the vestibular, visual and somatosensory systems. As part of the sensory reweighting mechanisms, vestibular activation exercises with headshaking influence vestibular-ocular reflex (VOR). However, combining challenging vestibular and postural tasks to facilitate more effective rehabilitation outcomes is under-utilized. Understanding how and why this may work is unknown. The aim of the study was to assess sensory reweighting of postural control processing and VOR after concurrent vestibular activation and weight shift training (WST) in healthy young adults. Forty-two participants (18–35years) were randomly assigned into four groups: No training/control (CTL), a novel visual feedback WST coupled with a concurrent, rhythmic active horizontal or vertical headshake activity (HHS and VHS), or the same WST with no headshake (NHS). Training was performed for five days. All groups performed baseline- and post-assessments using the video head impulse test, sensory organization test, force platform rotations and electro-oculography. Significantly decreased horizontal eye movement variability in the HHS group compared to the other groups suggests improved gaze stabilization ( p = .024). Significantly decreased horizontal VOR gain ( p = .040) and somatosensory downweighting ( p = .050) were found in the combined headshake groups (HHS and VHS) compared to the other two groups (NHS and CTL). The training also showed a significantly faster automatic postural response ( p = .003) with improved flexibility ( p = .010) in the headshake groups. The concurrent training influences oculomotor function and suggests improved gaze stabilization through vestibular recalibration due to adaptation and possibly habituation. The novel protocol could be modified into progressive functional activities that would incorporate gaze stabilization exercises. The findings may have implications for future development of vestibular rehabilitation protocols.

Background and Purpose This study was undertaken to examine vestibulo‐ocular reflex (VOR) characteristics in myotonic dystrophy type 1 (DM1) and type 2 (DM2) using video head impulse testing (vHIT). Methods VOR gain, refixation saccade prevalence, first saccade amplitude, onset latency, peak velocity, and duration were compared in DM1, DM2, age‐matched normal controls, and patients with peripheral and central vestibulopathies. Results Fifty percent of DM1 and 37.5% of DM2 patients demonstrated reduced VOR gain. Refixation saccade prevalence for horizontal canal (HC) and posterior canal (PC) was significantly higher in DM1 (101 ± 42%, 82 ± 47%) and DM2 (70 ± 45%, 61 ± 38%) compared to controls (40 ± 28% and 43 ± 33%, p < 0.05). The first saccade amplitudes and peak velocities were higher in HC and PC planes in DM1 and DM2 compared to controls (p < 0.05). HC slow phase eye velocity profiles in DM1 showed delayed peaks. The asymmetry ratio, which represents the percentage difference between the first and second halves of the slow phase eye velocity response, was therefore negative (−22.5 ± 17%, −2.3 ± 16%, and − 4.7 ± 8% in DM1, DM2, and controls). HC VOR gains were lower and gain asymmetry ratio was larger and negative in patients with DM1 with moderate to severe ptosis and a history of imbalance and falls compared to the remaining DM1 patients (p < 0.05). In peripheral vestibulopathies, saccade amplitude was larger, peak velocity was higher, and onset latency was shorter (p < 0.05) than in DM1. In central vestibulopathy (posterior circulation strokes), saccade peak velocity was higher, but amplitude and onset latency were not significantly different from DM1. Conclusions VOR impairment is common in DM1 and DM2. In DM1, refixation saccade characteristics are closer to central than peripheral vestibulopathies. Delayed peaks in the vHIT eye velocity profile observed in patients with DM1 may reflect extraocular muscle weakness. VOR impairment and VOR asymmetry in DM1 are associated with imbalance and falls.

Introduction Mal de Debarquement Syndrome (MdDS) is a rare central vestibular disorder characterised by a constant sensation of motion (rocking, swaying, bobbing), which typically arises after motion experiences (e.g. sea, air, and road travel), though can be triggered by non-motion events. The current standard of care is non-specific medications and interventions that only result in mild-to-moderate improvements. The vestibular ocular reflex (VOR) rehabilitation protocol, a specialised form of rehabilitation, has shown promising results in reducing symptoms amongst people with MdDS. Accumulating evidence suggests that it may be possible to augment the effects of VOR rehabilitation via non-invasive brain stimulation protocols, such as theta burst stimulation (TBS). Methods The aim of this randomised controlled trial was to evaluate the effectiveness of intermittent TBS (iTBS) over the dorsolateral prefrontal cortex in enhancing the effectiveness of a subsequently delivered VOR rehabilitation protocol in people with MdDS. Participants were allocated randomly to receive either Sham ( n  = 10) or Active ( n  = 10) iTBS, followed by the VOR rehabilitation protocol. Subjective outcome measures (symptom ratings and mental health scores) were collected 1 week pre-treatment and for 16 weeks post-treatment. Posturography (objective outcome) was recorded each day of the treatment week. Results Significant improvements in subjective and objective outcomes were reported across both treatment groups over time, but no between-group differences were observed. Discussion These findings support the effectiveness of the VOR rehabilitation protocol in reducing MdDS symptoms. Further research into iTBS is required to elucidate whether the treatment has a role in the management of MdDS. TRN: ACTRN12619001519145 (Date registered: 04 November 2019).

To investigate the influence of the amount of cervical movement on the cervico-ocular reflex (COR) and vestibulo-ocular reflex (VOR) in healthy individuals. Eye stabilization reflexes, especially the COR, are changed in neck pain patients. In healthy humans, the strength of the VOR and the COR are inversely related. In a cross-over trial the amplitude of the COR and VOR (measured with a rotational chair with eye tracking device) and the active cervical range of motion (CROM) was measured in 20 healthy participants (mean age 24.7). The parameters were tested before and after two different interventions (hyperkinesia: 20 min of extensive active neck movement; and hypokinesia: 60 min of wearing a stiff neck collar). In an additional replication experiment the effect of prolonged (120 min) hypokinesia on the eye reflexes were tested in 11 individuals. The COR did not change after 60 min of hypokinesia, but did increase after prolonged hypokinesia (median change 0.220; IQR 0.168, p = 0.017). The VOR increased after 60 min of hypokinesia (median change 0.155, IQR 0.26, p = 0.003), but this increase was gone after 120 min of hypokinesia. Both reflexes were unaffected by cervical hyperkinesia. Diminished neck movements influences both the COR and VOR, although on a different time scale. However, increased neck movements do not affect the reflexes. These findings suggest that diminished neck movements could cause the increased COR in patients with neck complaints.

In memory research, studying cerebellum-dependent memory is advantageous due to its relatively simple neural architecture compared with that of other memory circuits. To understand how cerebellum-dependent memory develops and is stored in this circuit, numerous hypotheses have been proposed. These hypotheses are generally able to adequately explain most learning and memory processes; however, several reported results are still poorly understood. Recently, the importance of intrinsic plasticity (i.e., plasticity of intrinsic excitability) has been highlighted in several studies. Because the classical view of cerebellum-dependent eye movement learning was focused on synaptic plasticity, it is valuable to consider the intrinsic plasticity for deeper understanding. In the present review, we re-examine the utility and limitations of previous hypotheses, from classic to recent, and propose an updated hypothesis. Integrating intrinsic plasticity into current models of the vestibulo-ocular reflex (VOR) circuit may facilitate deeper understanding of the VOR adaptation process. In particular, during the period of memory transfer, dynamic changes in excitability in both cerebellar Purkinje cells and vestibular nuclear neurons illuminate the role of intrinsic plasticity in the circuit.

Spinocerebellar ataxia type 6 (SCA6) homozygotes are known to have an earlier onset and faster disease progression than heterozygotes. Although several studies have reported more severe clinical manifestations in SCA6 homozygotes, longitudinal, quantitative assessments remain lacking. A 55-year-old female presented with intermittent positional dizziness/vertigo and gradually progressive gait disturbance. She denied a family history of similar symptoms. Neuro-ophthalmologic evaluations revealed spontaneous downbeat nystagmus, horizontal gaze-holding deficits and hypermetric saccades with preserved saccadic velocity. Bedside horizontal head impulses showed a perverted response. Video head impulse test (HIT) showed normal VOR gain in all six semicircular canals and bithermal caloric test was also normal. Brain magnetic resonance imaging (MRI) showed diffuse and prominent, pure cerebellar atrophy. Genetic testing for SCA using Sanger sequencing confirmed the expanded repeats for SCA6 with homozygous abnormal allele 20 repeats. During the 8-year follow-up, bedside HIT turned positive on both sides and accordingly decreased VOR gains with abnormal catch-up saccades in both horizontal canals (HCs) were detected during video HITs, while bithermal caloric test revealed canal paresis only on the right side. Follow-up brain MRI demonstrated more prominent diffuse cerebellar atrophy and indicated mild brainstem atrophy as well. Vestibular performance in SCA6 is characterized by frequent high-frequency angular VOR impairments, predominantly affecting the horizontal and posterior canals, while low-frequency responses remain variable. Neuro-otologic deterioration during follow-up in our patient may be partly attributed to involvement of the brainstem VOR pathway including the medial vestibular nuclei, in contrast to SCA6 heterozygotes who typically exhibit pure cerebellar involvement.

Vestibulo–ocular reflexes (VOR) are mediated by frequency-tuned pathways that separately transform the different dynamic and static aspects of head motion/position-related sensory signals into extraocular motor commands. Voltage-dependent potassium conductances such as those formed by Kv1.1 are important for the ability of VOR circuit elements to encode highly transient motion components. Here we describe the impact of the Kv1.1 channel blocker 4-aminopyridine (4-AP) on spontaneous and motion-evoked discharge of superior oblique motoneurons. Spike activity was recorded from the motor nerve in isolated preparations of Xenopus laevis tadpoles. Under static conditions, bath application of 1–10 µM 4-AP increased the spontaneous firing rate and provoked repetitive bursts of spikes. During motion stimulation 4-AP also augmented and delayed the peak firing rate suggesting that this drug affects the magnitude and timing of vestibular-evoked eye movements. The exclusive Kv1.1 expression in thick vestibular afferent fibers in larval Xenopus at this developmental stage suggests that the altered extraocular motor output in the presence of 4-AP mainly derives from a firing rate increase of irregular firing vestibular afferents that propagates along the VOR circuitry. Clinically and pharmacologically, the observed 4-AP-mediated increase of peripheral vestibular input under resting and dynamic conditions can contribute to the observed therapeutic effects of 4-AP in downbeat and upbeat nystagmus as well as episodic ataxia type 2, by an indirect increase of cerebellar Purkinje cell discharge.

Objective Validation of a bedside test to objectify the fixation suppression of the vestibulo-ocular reflex (FS-VOR) in patients with a cerebellar syndrome and healthy controls. Methods The vestibulo-ocular reflex and its fixation suppression were assessed by video-nystagmography (VNG) in 20 healthy subjects (mean age 56 ± 15) and 19 patients with a cerebellar syndrome (mean age 70 ± 11). The statistical cutoff delineating normal from pathological FS-VOR was determined at the 2.5th percentile of the normal distribution of the healthy cohort. VNG was then compared to a bedside test, where eye movements were recorded with a smartphone while patients were rotated on a swivel chair at a defined speed and amplitude. These videos were rated as normal or pathological FS-VOR by six blinded raters, and results compared to VNG. Results VNG in healthy controls showed FS-VOR with a reduction of nystagmus beats by 95.0% ± 7.2 (mean ± SD). The statistical cutoff was set at 80.6%. Cerebellar patients reduced nystagmus beats by only 26.3% ± 25.1. Inter-rater agreement of the smartphone video ratings was 85%. The sensitivity of the video ratings to detect an impaired FS-VOR was 99%, its specificity 92%. Inter-test agreement was 91%. Conclusion The smartphone bedside test is an easily performed, reliable, sensitive, specific, and inexpensive alternative for assessing FS-VOR.

One component of vestibular rehabilitation in patients with vestibulo-ocular reflex (VOR) hypofunction is gaze-stabilizing exercises that seek to increase (adapt) the VOR response. These prescribed home-based exercises are performed by the patient and thus their use/training is inherently variable. We sought to determine whether this variability affected VOR adaptation in ten healthy controls (× 2 training only) and ten patients with unilateral vestibular hypofunction (× 1 and × 2 training). During × 1 training, patients actively (self-generated, predictable) move their head sinusoidally while viewing a stationary fixation target; for × 2 training, they moved their outstretched hand anti-phase with their head rotation while attempting to view a handheld target. We defined the latter as manual × 2 training because the subject manually controls the target. In this study, head rotation frequency during training incrementally increased 0.5–2 Hz over 20 min. Active and passive (imposed, unpredictable) sinusoidal (1.3-Hz rotations) and head impulse VOR gains were measured before and after training. We show that for controls, manual × 2 training resulted in significant sinusoidal and impulse VOR adaptation of ~ 6 % and ~ 3 %, respectively, though this was ~two-thirds lower than increases after computer-controlled × 2 training (non-variable) reported in a prior study. In contrast, for patients, there was an increase in impulse but not sinusoidal VOR response after a single session of manual × 2 training. Patients had more than double the variability in VOR demand during manual × 2 training compared to controls, which could explain why adaptation was not significant in patients. Our data suggest that the clinical × 1 gaze-stabilizing exercise is a weak stimulus for VOR adaptation.

We sought to determine whether repeated vestibulo-ocular reflex (VOR) adaptation training to increase the VOR gain (eye/head velocity) had a lasting effect in normal subjects and whether there was a retinal image slip tolerance threshold for VOR adaptation. We used the unilateral incremental VOR adaptation technique and horizontal active (self-generated, predictable) head impulses as the vestibular stimulus. Both active and passive (imposed, unpredictable) head impulse VOR gains were measured before and after unilateral incremental VOR adaptation training. The adapting side was pseudo-randomized for left or right. We tested ten normal subjects over one block (10 sessions over 12 days) of VOR adaptation training and testing, immediately followed by a second block (5 sessions over 19 days) of testing only without training. Our findings show robust short-term VOR adaptation of ~ 10 % immediately after each 15-min training session, but that the daily pre-adaptation gain was most different on days 1 and 2, and for subsequent training days before saturating to ~ 5 % greater than the pre-adaptation gain on day 1. This increase was partially retained for 19 days after regular training stopped. The data suggest that stable vision in normal subjects is maintained when there is < 5 % deviation in VOR gain from the original baseline, which corresponds to < 9°/s retinal image slip. Below this threshold, there is poor adaptive drive to return the gain to its original baseline value.