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Due to their low cost and portability, using entertainment devices for indoor mapping applications has become a hot research topic. However, the impact of user behavior on indoor mapping evaluation with entertainment devices is often overlooked in previous studies. This article aims to assess the indoor mapping performance of entertainment devices under different mapping strategies. We chose two entertainment devices, the HoloLens 2 and iPhone 14 Pro, for our evaluation work. Based on our previous mapping experience and user habits, we defined four simplified indoor mapping strategies: straight-forward mapping (SFM), left-right alternating mapping (LRAM), round-trip straight-forward mapping (RT-SFM), and round-trip left-right alternating mapping (RT-LRAM). First, we acquired triangle mesh data under each strategy with the HoloLens 2 and iPhone 14 Pro. Then, we compared the changes in data completeness and accuracy between the different devices and indoor mapping applications. Our findings show that compared to the iPhone 14 Pro, the triangle mesh accuracy acquired by the HoloLens 2 has more stable performance under different strategies. Notably, the triangle mesh data acquired by the HoloLens 2 under the RT-LRAM strategy can effectively compensate for missing wall and floor surfaces, mainly caused by furniture occlusion and the low frame rate of the depth-sensing camera. However, the iPhone 14 Pro is more efficient in terms of mapping completeness and can acquire a complete triangle mesh more quickly than the HoloLens 2. In summary, choosing an entertainment device for indoor mapping requires a combination of specific needs and scenes. If accuracy and stability are important, the HoloLens 2 is more suitable; if efficiency and completeness are important, the iPhone 14 Pro is better.

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Several prior studies, including those from this laboratory, have suggested that vestibulo-ocular reflex (VOR) adaptation and compensation are two neurologically related mechanisms. We therefore hypothesised that adaptation would be affected by compensation, depending on the amount of overlap between these two mechanisms. To better understand this overlap, we examined the effect of gain-increase (gain = eye velocity/head velocity) adaptation training on the VOR in compensated mice since both adaptation and compensation mechanisms are presumably driving the gain to increase. We tested 11 cba129 controls and 6 α9-knockout mice, which have a compromised efferent vestibular system (EVS) known to affect both adaptation and compensation mechanisms. Baseline VOR gains across frequencies (0.2 to 10 Hz) and velocities (20 to 100°/s) were measured on day 28 after unilateral labyrinthectomy (UL) and post-adaptation gains were measured after gain-increase training on day 31 post-UL. Our findings showed that after chronic compensation gain-increase adaptation, as a percentage of baseline, in both strains of mice (~14%), was about half compared to their previously reported healthy, non-operated counterparts (~32%). Surprisingly, there was no difference in gain-increase adaptation between control and α9-knockout mice. These data support the notion that adaptation and compensation are separate but overlapping processes. They also suggest that half of the original adaptation capacity remained in chronically compensated mice, regardless of EVS compromise associated with α9-knockout mice, and strongly suggest VOR adaptation training is a viable treatment strategy for vestibular rehabilitation therapy and, importantly, augments the compensatory process.

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Genioglossus was stimulated intramuscularly to determine the effect of regional activation of the muscle on tongue movement in eight healthy adults. Stimulation at motor threshold was delivered with a needle electrode inserted to different depths in the anterior and posterior regions of genioglossus. The current amplitude that induced muscle contraction was ∼80% higher for anterior than posterior sites. Evoked tongue movements were determined from stimulus-triggered averages (150 pulses) of the outputs from an accelerometer fixed to the posterosuperior surface of the tongue. The median amplitude [95% confidence intervals] for the resultant acceleration was 0.0 m/s2 [0.0, 0.2] for anterior and 0.6 m/s2 [0.1, 2.8] for posterior sites. There was a positive relationship between acceleration amplitude and stimulation depth in the posterior of genioglossus (p < 0.001), but acceleration amplitude did not vary with stimulation depth in the anterior region (p = 0.83). This heterogeneity in acceleration responses between muscle regions may contribute to differences in collapsibility of the upper airway.

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Cochlear implants are very well established in the rehabilitation of hearing loss and are regarded as the most successful neuroprostheses to date. While a lot of progress has also been made in the neighboring field of specific vestibular implants, some diseases affect the entire inner ear, leading to both hearing and vestibular hypo- or dysfunction. The proximity of the cochlear and vestibular organs suggests a single combined implant as a means to alleviate the associated impairments. While both organs can be stimulated in a similar way with electric pulses applied through implanted electrodes, the typical phase durations needed in the vestibular system seem to be substantially larger than those typically needed in the cochlear system. Therefore, when using sequential stimulation in a combined implant, the pulse stream to the cochlea is interrupted by comparatively large gaps in which vestibular stimulation can occur. We investigate the impact of these gaps in the auditory stream on speech perception. Specifically, we compare a number of stimulation strategies with different gap lengths and distributions and evaluate whether it is feasible to use them without having a noticeable decline in perception and quality of speech. This is a prerequisite for any practicable stimulation strategy of a combined system and can be investigated even in recipients of a normal cochlear implant. Our results show that there is no significant deterioration in speech perception for the different strategies examined in this paper, leaving the strategies as viable candidates for prospective combined cochleo-vestibular implants.

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People aged over 50 are the most likely to present to a physician for dizziness. It is important to identify the main cause of dizziness in order to develop the best treatment approach. Our goal was to determine the prevalence of benign paroxysmal positional vertigo (BPPV), and peripheral and central vestibular function in people that had experienced dizziness within the past year aged over 50. One hundred and ninety three community-dwelling participants aged 51-92 (68 ± 8.7 years; 117 females) were tested using the clinical and video head impulse test (cHIT and vHIT) to test high-frequency vestibular organ function; the head thrust dynamic visual acuity (htDVA) test to test high-frequency visual-stability; the dizziness handicap inventory (DHI) to measure the impact of dizziness; as well as sinusoidal and unidirectional rotational chair testing to test low- to mid-frequency peripheral and central vestibular function. From these assessments we computed the following measures: HIT gain; htDVA score; DHI score; sinusoidal (whole-body; 0.1-2 Hz with 30°/s peak-velocity) vestibulo-ocular reflex (VOR) gain and phase; transient (whole-body, 150°/s2 acceleration to 50°/s constant velocity) VOR gain and time constant; optokinetic nystagmus (OKN) gain and time constant (whole-body, 50°/s constant velocity rotation). Our study showed that BPPV, and peripheral or central vestibular hypofunction were present in 34% of participants, suggesting a vestibular cause to their dizziness. Over half (57%) of these with a likely vestibular cause had BPPV, which is more than twice the percentage reported in other dizzy clinic studies. Our findings suggest that the physical DHI score and VOR time constant were best at detecting those with non-BPPV vestibular loss, but should always be used in conjunction with cHIT or vHIT, and that the htDVA score and vHIT gain were best at detecting differences between ipsilesional and contralesional sides.

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The Microsoft HoloLens is a head-worn mobile augmented reality device that is capable of mapping its direct environment in real-time as triangle meshes and localize itself within these three-dimensional meshes simultaneously. The device is equipped with a variety of sensors including four tracking cameras and a time-of-flight (ToF) range camera. Sensor images and their poses estimated by the built-in tracking system can be accessed by the user. This makes the HoloLens potentially interesting as an indoor mapping device. In this paper, we introduce the different sensors of the device and evaluate the complete system in respect of the task of mapping indoor environments. The overall quality of such a system depends mainly on the quality of the depth sensor together with its associated pose derived from the tracking system. For this purpose, we first evaluate the performance of the HoloLens depth sensor and its tracking system separately. Finally, we evaluate the overall system regarding its capability for mapping multi-room environments.

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The vestibulo-ocular reflex (VOR) is the primary mechanism for stabilizing vision during rapid head movements. We have developed a training technique that typically increases the VOR response a minimum of 15% after 15 mins of training. This technique relies on subjects tracking a visual target that moves as a function of head motion, but at a different speed, so that the VOR is challenged to increase in order to stabilize the retinal image of the target. We have developed a portable device, StableEyes, which implements this technique so that unassisted training can be performed at home by patients with VOR hypofunction. The device consists of a head unit and base unit. The head unit contains inertial sensors to measure the instantaneous 3-D orientation of the head in space at 250 Hz, and an integrated circuit mirror to dynamically control the position of a laser target in space. The base unit consists of a touch screen interface that allows users to calibrate and set the device, in addition to recording compliance. The laser target range is ±12.5°. The device latency is 6 ms with a frequency response stable up to 6 Hz for velocities >80°/s, i.e., head velocities, where the VOR contributes most to visual stability. StableEyes was used to increase the VOR response in 10 normal subjects. In these, the VOR towards the adapting side increased by ~11%, which is comparable to our laboratory findings. The adoption of StableEyes could improve the efficacy of vestibular rehabilitation and its outcomes.

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Core body temperature has been shown to affect vestibular end-organ and nerve afferents so that their resting discharge rate and sensitivity increase with temperature. Our aim was to determine whether these changes observed in extracellular nerve recordings of anaesthetized C57BL/6 mice corresponded to changes in the behavioural vestibulo-ocular reflex (VOR) of alert mice. The VOR drives eye rotations to keep images stable on the retina during head movements. We measured the VOR gain (eye velocity/head velocity) and phase (delay between vestibular stimulus and response) during whole-body sinusoidal rotations ranging 0.5-12 Hz with peak velocity 50 or 100 °/s in nine adult C57BL/6 mice. We also measured the VOR during whole-body transient rotations with acceleration 3000 or 6000 °/s2 reaching a plateau of 150 or 300 °/s. These measures were obtained while the mouse's core body temperature was held at either 32 or 37 °C for at least 35 min before recording. The temperature presentation order and timing were pseudo-randomized. We found that a temperature increase from 32 to 37 °C caused a significant increase in sinusoidal VOR gain of 17 % (P < 0.001). Temperature had no other effects on the behavioural VOR. Our data suggest that temperature effects on regularly firing afferents best correspond to the changes that we observed in the VOR gain.

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The α9-nicotinic acetylcholine receptor (α9-nAChR) subunit is expressed in the vestibular and auditory periphery, and its loss of function could compromise peripheral input from the predominantly cholinergic efferent vestibular system (EVS). A recent study has shown that α9-nAChRs play an important role in short-term vestibulo-ocular reflex (VOR) adaptation. We hypothesize that α9-nAChRs could also be important for other forms of vestibular plasticity, such as that needed for VOR recovery after vestibular organ injury. We measured the efficacy of VOR compensation in α9 knockout mice. These mice have deletion of most of the gene (chrna9) encoding the nAChR and thereby lack α9-nAChRs. We measured the VOR gain (eye velocity/head velocity) in 20 α9 knockout mice and 16 cba129 controls. We measured the sinusoidal (0.2-10 Hz, 20-100°/s) and transient (1,500-6,000°/s2) VOR in complete darkness before (baseline) unilateral labyrinthectomy (UL) and then 1, 5, and 28 days after UL. On day 1 after UL, cba129 mice retained ~50% of their initial function for contralesional rotations, whereas α9 knockout mice only retained ~20%. After 28 days, α9 knockout mice had ~50% lower gain for both ipsilesional and contralesional rotations compared with cba129 mice. Cba129 mice regained ~75% of their baseline function for ipsilesional and ~90% for contralesional rotations. In contrast, α9 knockout mice only regained ~30% and ~50% function, respectively, leaving the VOR severely impaired for rotations in both directions. Our results show that loss of α9-nAChRs severely affects VOR compensation, suggesting that complimentary central and peripheral EVS-mediated adaptive mechanisms might be affected by this loss.NEW & NOTEWORTHY Loss of the α9-nicotinic acetylcholine receptor (α9-nAChR) subunit utilized by the efferent vestibular system (EVS) has been shown to significantly affect vestibulo-ocular reflex (VOR) adaptation. In our present study we have shown that loss of α9-nAChRs also affects VOR compensation, suggesting that the mammalian EVS plays an important role in vestibular plasticity, in general, and that VOR compensation is a more distributed process than previously thought, relying on both central and peripheral changes.

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Prevailing evidence indicates a relatively late life decline in human vestibulo-ocular reflex (VOR) function. Although mice are commonly used in mechanistic studies of vestibular function, it remains unclear whether aging produces a corresponding decline in VOR function in mice. We sought to determine how the baseline VOR and its short-term adaptation were affected by aging. We tested 8 young (3-month old) and 8 aged (30-month old-equivalent to a ∼80-year old human) C57BL/6 mice. We measured their VOR response to whole-body static tilts and during 0.1-10 Hz whole-body sinusoidal and transient rotations before and after VOR adaptation training. Our data revealed minimal differences in static counter-tilt response between young and aged mice, but a significant deficit in baseline VOR gain in aged mice during transient rotations. Moreover, aged mice had a significant decrease in short-term VOR adaptation, particularly for training that sought to decrease the VOR response.

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Although anatomically well described, the functional role of the mammalian efferent vestibular system (EVS) remains unclear. Unlike in fish and reptiles, the mammalian EVS does not seem to play a role in modulation of primary afferent activity in anticipation of active head movements. However, it could play a role in modulating long-term mechanisms requiring plasticity such as vestibular adaptation. We measured the efficacy of vestibuloocular reflex (VOR) adaptation in α9-knockout mice. These mice carry a missense mutation of the gene encoding the α9 nicotinic acetylcholine receptor (nAChR) subunit. The α9 nAChR subunit is expressed in the vestibular and auditory periphery, and its loss of function could compromise peripheral input from the predominantly cholinergic EVS. We measured the VOR gain (eye velocity/head velocity) in 26 α9-knockout mice and 27 cba129 control mice. Mice were randomly assigned to one of three groups: gain-increase adaptation (1.5×), gain-decrease adaptation (0.5×), or no adaptation (baseline, 1×). After adaptation training (horizontal rotations at 0.5 Hz with peak velocity 20°/s), we measured the sinusoidal (0.2-10 Hz, 20-100°/s) and transient (1,500-6,000°/s(2)) VOR in complete darkness. α9-Knockout mice had significantly lower baseline gains compared with control mice. This difference increased with stimulus frequency (∼ 5% <1 Hz to ∼ 25% >1 Hz). Moreover, vestibular adaptation (difference in VOR gain of gain-increase and gain-decrease adaptation groups as % of gain increase) was significantly reduced in α9-knockout mice (17%) compared with control mice (53%), a reduction of ∼ 70%. Our results show that the loss of α9 nAChRs moderately affects the VOR but severely affects VOR adaptation, suggesting that the EVS plays a crucial role in vestibular plasticity.

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Dizziness and imbalance are clinically poorly defined terms, which affect ~30% of people over 65 years of age. In these people, it is often difficult to define the primary cause of dizziness, as it can stem from cardiovascular, vestibular, psychological, and neuromuscular causes. However, identification of the primary cause is vital in determining the most effective treatment strategy for a patient. Our aim is to accurately identify the prevalence of benign paroxysmal positional vertigo (BPPV), peripheral, and central vestibular hypofunction in people aged over 50 years who had experienced dizziness within the past year. Seventy-six participants aged 51-92 (mean ± SD = 69 ± 9.5 years) were tested using the head thrust dynamic visual acuity (htDVA) test, dizziness handicap inventory (DHI), as well as sinusoidal and unidirectional rotational chair testing, in order to obtain data for htDVA score, DHI score, sinusoidal (whole-body, 0.1-2 Hz with peak velocity at 30°/s) vestibulo-ocular reflex (VOR) gain and phase, transient (whole-body, acceleration at 150°/s(2) to a constant velocity rotation of 50°/s) VOR gain and time constant (TC), optokinetic nystagmus (OKN) gain, and TC (whole-body, constant velocity rotation at 50°/s). We found that BPPV, peripheral and central vestibular hypofunction were present in 38 and 1% of participants, respectively, suggesting a likely vestibular cause of dizziness in these people. Of those with a likely vestibular cause, 63% had BPPV; a figure higher than previously reported in dizziness clinics of ~25%. Our results indicate that htDVA, sinusoidal (particularly 0.5-1 Hz), and transient VOR testing were the most effective at detecting people with BPPV or vestibular hypofunction, whereas DHI and OKN were effective at only detecting non-BPPV vestibular hypofunction.

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One commonly observed phenomenon of vestibulo-ocular reflex (VOR) adaptation is a frequency-selective change in gain (eye velocity/head velocity) and phase (relative timing between the vestibular stimulus and response) based on the frequency content of the adaptation training stimulus. The neural mechanism behind this type of adaptation is not clear. Our aim was to determine whether there were other parameter-selective effects on VOR adaptation, specifically velocity-selective and acceleration-selective changes in the horizontal VOR gain and phase. We also wanted to determine whether parameter selectivity was also in place for cross-axis adaptation training (a visual-vestibular training stimulus that elicits a vestibular-evoked torsional eye movement during horizontal head rotations). We measured VOR gain and phase in 17 C57BL/6 mice during baseline (no adaptation training) and after gain-increase, gain-decrease and cross-axis adaptation training using a sinusoidal visual-vestibular (mismatch) stimulus with whole-body rotations (vestibular stimulus) with peak velocity 20 and 50°/s both with a fixed frequency of 0.5 Hz. Our results show pronounced velocity selectivity of VOR adaptation. The difference in horizontal VOR gain after gain-increase versus gain-decrease adaptation was maximal when the sinusoidal testing stimulus matched the adaptation training stimulus peak velocity. We also observed similar velocity selectivity after cross-axis adaptation training. Our data suggest that frequency selectivity could be a manifestation of both velocity and acceleration selectivity because when one of these is absent, e.g. acceleration selectivity in the mouse, frequency selectivity is also reduced.

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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.

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