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Unilateral or bilateral vestibular hypofunction presents most commonly with symptoms of dizziness or postural imbalance and affects a large population. However, it is often missed because no quantitative testing of vestibular function is performed, or misdiagnosed due to a lack of standardization of vestibular testing. Therefore, this article reviews the current status of the most frequently used vestibular tests for canal and otolith function. This information can also be used to reach a consensus about the systematic diagnosis of vestibular hypofunction.

Throughout Bernard Cohen's active career at Mount Sinai that lasted over a half century, he was involved in research on vestibular control of the oculomotor, body postural, and autonomic systems in animals and humans, contributing to our understanding of such maladies as motion sickness, mal de débarquement syndrome, and orthostatic syncope. This review is an attempt to trace and connect Cohen's varied research interests and his approaches to them. His influence was vast. His scientific contributions will continue to drive research directions for many years to come.

Objective The video head impulse test (vHIT) is a diagnostic tool to assess the function of the semicircular canals and branches of the vestibular nerve. The aim of this study was to analyze the interexaminer variability of vHIT results in healthy subjects. Materials and Methods A total of 21 healthy participants were included in the study. vHIT responses were collected by four clinicians. Variability of the vHIT results between examiners was analyzed statistically. Results The vestibulo-ocular reflex (VOR) velocity regression values were from 0.99 to 1.09 degrees per second for the lateral canals. For the vertical canals, VOR velocity regression values were from 0.87 to 1.21 degrees per second. According to repeated measures analysis of variance, the normality assumptions for the velocity regression of the left lateral canal (p = 0.002) and the right anterior canal (p Conclusion The interexaminer differences of the VOR gain values for the vHIT were statistically significant. Serial vHIT testing should be performed by the same examiner to reduce the effects of interexaminer variability.

PURPOSE OF REVIEW In the last decades, researchers suggested that clinical assessment of labyrinthine function in detail became easy thanks to video head impulse tests (VHITs), vestibular evoked myogenic potential test (VEMP) and video-oculography (VOG). It has been argued that they can replace electronystagmography, the caloric and rotatory chair tests. This review addresses the latest evaluations of these tests and the opportunities they offer, but also the limitations in clinical practice. RECENT FINDINGS The VHIT and suppression head impulse test (SHIMP) are under ideal circumstances able to accurately identify deficits of the VOR in 3D. However, in a relevant part of the patient population, pupil tracking is inaccurate, video-goggles slip and VOR quantification is problematic. The dissociation between the VHIT and caloric test suggests that these tests are complementary. A new 3D-VOG technique claims to quantify eye torsion better than before, opening multiple diagnostic possibilities. VEMPs remain difficult to standardize. Variability in normal cervical vestibular-evoked myogenic potential amplitude is large. VEMPs become smaller or absent with age, raising questions of whether there is a lower normal limit at all. Recent research shows that the labyrinth is directly stimulated in the MRI offering new opportunities for diagnostics and research. SUMMARY In clinical practice, the VHIT, SHIMP, VEMP and new 3D-VOG techniques improve diagnostic power. Unfortunately, technical issues or variability prevent reliable quantitative evaluation in a part of the regular patient population. The traditional caloric and rotatory chair test can still be considered as valuable complementary tests.

In the interaural direction, translational linear acceleration is loaded during lateral translational movement and gravitational acceleration is loaded during lateral tilting movement. These two types of acceleration induce eye movements via two kinds of otolith-ocular reflexes to compensate for movement and maintain clear vision: horizontal eye movement during translational movement, and torsional eye movement (torsion) during tilting movement. Although the two types of acceleration cannot be discriminated, the two otolith-ocular reflexes can distinguish them effectively. In the current study, we tested whether lateral-eyed mice exhibit both of these otolith-ocular reflexes. In addition, we propose a new index for assessing the otolith-ocular reflex in mice. During lateral translational movement, mice did not show appropriate horizontal eye movement, but exhibited unnecessary vertical torsion-like eye movement that compensated for the angle between the body axis and gravito-inertial acceleration (GIA; i.e., the sum of gravity and inertial force due to movement) by interpreting GIA as gravity. Using the new index (amplitude of vertical component of eye movement)/(angle between body axis and GIA), the mouse otolith-ocular reflex can be assessed without determining whether the otolith-ocular reflex is induced during translational movement or during tilting movement.

Introduction A horizontal vestibulo-ocular reflex gain (VOR gain) of Methods This study comprised 46 BV patients (diagnosed according to the Báràny criteria), tested with three commercial VHIT systems (Interacoustics, Otometrics and Synapsys) in random order. Main outcome parameter was VOR gain as calculated by the system, and the agreement on BV diagnosis (VOR gain Results VOR gain in the Synapsys system differed significantly from VOR gain in the other two systems [F(1.256, 33.916) = 35.681, p Conclusion To conclude, using different VHIT systems in the same BV patient can lead to clinically significant differences in VOR gain, when using a cut-off value of 0.6. This might hinder proper diagnosis of BV patients. It would, therefore, be preferred that VHIT systems are standardised regarding eye and head tracking methods, and VOR gain calculation algorithms. Until then, it is advised to not only take the VOR gain in consideration when assessing a VHIT trial, but also look at the raw traces and the compensatory saccades.

Aim: To evaluate if patients with Mal de Debarquement syndrome (MdDS) demonstrate different symptom levels or symptom type during pregnancy. Materials & methods: 18 MdDS patients that were or had been pregnant during their condition were recruited to complete a retrospective online questionnaire. Respondents answered questions regarding their basic clinical data, diagnosis, triggers and differences in symptom level and symptom type during pregnancy and before pregnancy. Results: A total of 81.3% reported that their symptoms were reduced during pregnancy compared with before pregnancy. Respondents also reported a different perception of motion and experienced less dizziness while being pregnant. Conclusion: The physiological changes that occur during pregnancy improve the symptoms of patients with MdDS, and this is potentially attributable to the rise in estrogen and progesterone., Lay abstract Mal de Debarquement syndrome (MdDS) is a rare neurological disorder characterized by a constant sensation of self-motion. More women are affected than men, and subsequently a hormonal implication has been theorized. This study aimed to evaluate if symptoms change in patients with MdDS during their pregnancy. A total of 18 MdDS patients were recruited to complete a retrospective online questionnaire. Among these, 81.3% of respondents reported that their symptoms were lower during pregnancy compared with before pregnancy. Respondents also reported a different perception of motion and experienced less dizziness while being pregnant. Our results support the hypothesis that pregnancy positively influences MdDS symptoms.

The cerebellum was historically considered a brain region dedicated to motor control, but it has become clear that it also contributes to sensory processing, particularly when sensory discrimination is required. Prior work, for example, has demonstrated a cerebellar contribution to sensory discrimination in the visual and auditory systems. The cerebellum also receives extensive inputs from the motion and gravity sensors in the vestibular labyrinth, but its role in the perception of head motion and orientation has received little attention. Drawing on the lesion-deficit approach to understanding brain function, we evaluated the contributions of the cerebellum to head motion perception by measuring perceptual thresholds in two subjects with congenital agenesis of the cerebellum. We used a set of passive motion paradigms that activated the semicircular canals or otolith organs in isolation or combination, and compared results of the agenesis patients with healthy control subjects. Perceptual thresholds for head motion were elevated in the agenesis subjects for all motion protocols, most prominently for paradigms that only activated otolith inputs. These results demonstrate that the cerebellum increases the sensitivity of the brain to the motion and orientation signals provided by the labyrinth during passive head movements.

The aim of this study was to develop software that performs the optokinetic tracking assessment without the involvement of experimenters to increase the objectivity of the test. To check the effectiveness of the software, several videos were analyzed and the results were compared to those produced by two experimenters. Videos consisted of visual acuity and contrast sensitivity tests on normal animals and pigmented P23H rats (animal model of retinitis pigmentosa). Our software showed a reasonably high success rate: in approximately 78% of the cases, both the software program and the experimenters were in agreement, including the direction of rotation. The software detected 7% false positive cases, 10% false negative cases, and it was wrong in 5% of the cases. Decrease in visual function with age in pigmented P23H rats was observed from the first time interval, although minimum thresholds were found in visual parameters at advanced ages. We developed simple software based on current functions included in the Matlab image processing toolbox that was able to recognize, with a reasonably high percentage of success, the subtle head movements of the rodent produced when visual perception of the optokinetic optotype occurs Publication of this article was supported by the General Council of Aragon (Diputación General de Aragón) Group B99, Health Research Fund Instituto de Salud Carlos III (Fondo de Investigación Sanitaria, Spanish Ministry of Health) PI13/01124, and Health Institute Carlos III (Instituto de Salud Carlos III) RETICS RD16/0008/0016, ED431B 2017/64 (Xunta de Galicia and FEDER), and FIS2016–77319 (Ministerio de Industria, Economía y Competitividad and FEDER) SI

The increased use of close range explosives has led to a higher incidence of exposure to blast-related head trauma. Exposure to primary blast waves is a significant cause of morbidity and mortality. Active service members and civilians who have experienced blast waves report high rates of vestibular dysfunction, such as vertigo, oscillopsia, imbalance, and dizziness. Accumulating evidence suggests that exposure to blast-wave trauma produces damage to both the peripheral and central vestibular system; similar to previous findings that blast exposure results in damage to auditory receptors. In this study, mice were exposed to a 63 kPa peak blast-wave over pressure and were examined for vestibular receptor damage as well as behavioral assays to identify vestibular dysfunction. We observed perforations to the tympanic membrane in all blast animals. We also observed significant loss of stereocilia on hair cells in the cristae and macule up to 1 month after blast-wave exposure; damage that is likely permanent. Significant reductions in the ability to perform the righting reflex and balance on a rotating rod that lasted several weeks after blast exposure were prominent behavioral effects. We also observed a significant reduction in horizontal vestibuloocular reflex gain and phase lags in the eye movement responses that lasted many weeks following a single blast exposure event. OKN responses were absent immediately following blast exposure, but began to return after several weeks’ recovery. These results show that blast-wave exposure can lead to peripheral vestibular damage (possibly central deficits as well) and provides some insight into causes of vestibular dysfunction in blast-trauma victims.

OBJECTIVE: To explore clinical features of patients with bilateral vestibular hypofunction (BVH) verified in motorized head impulse test (MHIT). MATERIALS and METHODS: We examined clinical records of 23 adult patients (10 males and 13 females), whose gain of the vestibulo-ocular reflex in the MHIT was bilaterally lowered. Fifteen of 62 unilateral cochlear implant (CI) recipients routinely tested both pre-and postoperatively with the MHIT had BVH. Eight of 198 vestibular outpatients selected to the MHIT due to clinical causes had BVH. Clinical characteristics and a questionnaire regarding current sensations were analyzed. RESULTS: The mean gain +/- SD in the MHIT was 0.26 +/- 0.17 on the right and 0.26 +/- 0.14 on the left side. The mean gain in the CI recipients did not differ from that of vestibular outpatients (p>0.05). All outpatients with BVH suffered from oscillopsia, whereas only 46% of CI recipients experienced oscillopsia (p=0.048). Instability was more prominent (p=0.004) and quality of life further decreased (p=0.012) among vestibular outpatients compared with CI patients. Most common etiology for the BVH was meningitis. Other causes were either sudden or progressive loss of labyrinthine function, bilateral Meniere's disease, and ototoxicity. CONCLUSION: BVH is rare even in a specialized clinic. Vestibular outpatients were more disabled than CI recipients with the BVH.

The purpose of this study was to evaluate whether it is possible to restore the high-frequency angular vestibulo-ocular reflex (aVOR) in patients suffering from a severe bilateral vestibulopathy (BV) and implanted with a vestibular implant prototype. Three patients (S1-3) participated in the study. They received a prototype vestibular implant with one to three electrode branches implanted in the proximity of the ampullary branches of the vestibular nerve. Five electrodes were available for electrical stimulation: one implanted in proximity of the left posterior ampullary nerve in S1, one in the left lateral and another one in the superior ampullary nerves in S2, and one in the right lateral and another one in the superior ampullary nerves in S3. The high-frequency aVOR was assessed using the video head impulse test (EyeSeeCam; EyeSeeTec, Munich, Germany), while motion-modulated electrical stimulation was delivered via one of the implanted vestibular electrodes at a time. aVOR gains were compared to control measurements obtained in the same patients when the device was not activated. In three out of the five tested electrodes the aVOR gain increased monotonically with increased stimulation strength when head impulses were delivered in the plane of the implanted canal. In these cases, gains ranging from 0.4 to values above 1 were measured. A "reversed" aVOR could also be generated when inversed stimulation paradigms were used. In most cases, the gain for excitatory head impulses was superior to that recorded for inhibitory head impulses, consistent with unilateral vestibular stimulation. Improvements of aVOR gain were generally accompanied by a concomitant decrease of corrective saccades, providing additional evidence of an effective aVOR. High inter-electrode and inter-subject variability were observed. These results, together with previous research, demonstrate that it is possible to restore the aVOR in a broad frequency range using motion-modulated electrical stimulation of the vestibular afferents. This provides additional encouraging evidence of the possibility of achieving a useful rehabilitation alternative for patients with BV in the near future.

Background: The present study investigated whether prochlorperazine affects vestibulo-ocular reflex (VOR) and vestibulo-perceptual function. Methods: We studied 12 healthy naïve subjects 3 h after a single dose of oral prochlorperazine 5 mg in a randomised, placebo-controlled, double-blind, crossover study in healthy young subjects. Two rotational tests in yaw were used: (1) a threshold task investigating perceptual motion detection and nystagmic thresholds (acceleration steps of 0.5°/s2) and (2) suprathreshold responses to velocity steps of 90°/s in which vestibulo-ocular and vestibuloperceptual time constants of decay, as well as VOR gain, were measured. Results: Prochlorperazine had no effect upon any measure of nystagmic or perceptual vestibular function compared to placebo. This lack of effects on vestibular-mediated motion perception suggests that the drug is likely to act more as an anti-emetic than as an antivertiginous agent.

Introduction Unilateral labyrinthectomy and intra-tympanic gentamycin have been employed in the treatment of Ménière's disease, but the efficacy of these techniques has not been well established. Objective The objective of this study is to measure the time course of recovery from a unilateral labyrinthectomy either after ipsilateral topical treatment with gentamicin to the inner ear or without the previous insult. Methods Twenty-nine adult Mongolian gerbils were randomized into two experimental groups. Group 1 (n = 17) received a right ear gentamicin drug-induced lesion by unilateral labyrinthectomy (UL). Group 2 (n = 12) only received a right unilateral labyrinthectomy lesion. We measured the horizontal vestibulo-ocular responses in gerbils before and after the lesion. The gerbils received an angular acceleration stimulus and their eye movements were recorded. Results The gentamicin lesion resulted in a quicker recovery. Experimental groups underwent a similar time course of recovery. Statistical analysis showed no significant difference between the two groups. Both groups displayed adaptation to the lesion by day 21, but long-term compensation did not completely revert to the original pre-lesion state. Conclusions In a lesion requiring both static and dynamic compensation as in UL, the need for a static compensation may alter pre-existing compensation from a previous dynamic insult and require a new compensation. A previous lesion and adaptation is not preserved for a second lesion and the subject has to re-compensate. Therefore, surgical treatment in Meniere's disease such as UL can be considered without prior gentamicin treatment. Static and dynamic compensations do not appear to be as independent as previous studies have suggested.

The cerebellum aids the learning and execution of fast coordinated movements, with acquired information being stored by plasticity of parallel fibre—Purkinje cell synapses. According to the current consensus, erroneously active parallel fibre synapses are depressed by complex spikes arising when climbing fibres signal movement errors. However, this theory cannot solve the credit assignment problem of using the limited information from a global movement evaluation to optimise behaviour by guiding the plasticity in numerous neurones. We identify the possible implementation of an algorithm solving this problem, whereby spontaneous complex spikes perturb ongoing movements, create an eligibility trace for plasticity and signal resulting error changes to guide plasticity. These error changes are extracted by adaptively cancelling the average error. This framework, stochastic gradient descent with estimated global errors, generates specific predictions for synaptic plasticity rules that contradict the current consensus. However, in vitro plasticity experiments under physiological conditions verified our predictions, highlighting the sensitivity of plasticity studies to unphysiological conditions. Using numerical and analytical approaches we demonstrate the convergence and estimate the capacity of learning in our implementation. Finally, a similar mechanism may operate during optimisation of action sequences by the basal ganglia, where dopamine could both initiate movements and signal rewards, analogously to the dual perturbation and correction role of the climbing fibre outlined here.

The handicap resulting from a bilateral vestibular deficit is often underestimated. In most cases the deficit settles gradually. Patients do not understand what is happening to them and have many difficulties to describe their symptoms. They have to consult several doctors with different medical specialties before diagnosis. Once the diagnosis is made there is no biological way to "repair'' the deficient vestibular apparatus and vestibular exercises are mildly effective. Attempts have been made to help patients using substitution devices replacing the defective vestibular information by tactile or acoustic cues. Currently, efforts are being made towards the development of a vestibular implant, conceptually similar to the cochlear implant for the rehabilitation of deaf patients. In recent years, several experiments on animal models have demonstrated the feasibility of this project. This paper reports the steps accomplished in human experiments and the main results obtained in our laboratory.

Objective: Bone-conducted vibration (BCV) in the midline at the hairline (Fz), results in short latency potentials recorded by surface electrodes beneath the eyes - the ocular vestibular-evoked myogenic potential (oVEMP). The early negative component of the oVEMP, n10, is due to vestibular stimulation, however it is similar to the early R1 component of the blink reflex. Here we seek to dissociate n10 from R1. Methods: Surface potentials were recorded from the infraorbital electromyogram of 10 healthy subjects, 6 patients with bilateral vestibular loss, 2 with unilateral vestibular loss, 4 with facial palsy and 3 with facial and vestibular nerve lesions on the same side. BCV was delivered at Fz, the inion, the glabella or the supra-orbital ridge using a tendon hammer or a bone-conduction vibrator. Results: Onset latencies of the n10 evoked by taps at Fz or inion were significantly shorter than the R1 components of blink responses to supraorbital and glabellar stimuli. Upward gaze increased the amplitude of The n10 was absent bilaterally in patients with bilateral vestibular loss and beneath the contralesional eye in patients with unilateral vestibular loss, but in both these groups of patients R1 was preserved. In severe facial palsy the R1 component was absent or delayed and attenuated ipsilesionally, but n10 was preserved bilaterally. In subjects with unilateral facial and vestibular nerve lesions (Herpes Zoster of the facial and vestibulocochlear nerves) the dissociation was complete - the ipsilesional R1 was absent or attenuated whereas the ipsilesional n10 was preserved. Conclusions: n10 is distinguished from R1 by its earlier onset, laterality, modulation by gaze position and dissociation in patient groups. Significance: The n10 component evoked by BCV at Fz is not the R1 component of the blink reflex. (C) 2009 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

In the lamb, acute unilateral section of the ophthalmic branch induced in the ipsilateral eye occasional oscillations of the resting position and misalignment of the horizontal vestibulo-ocular reflex (HVOR) with respect to the stimulus. Additional electrolytic lesion of the cells innervating the proprioceptors of the medial rectus muscle, or of the lateral rectus muscle in the contralateral semilunar ganglion, provoked a 4 degrees-7 degrees consensual eye deviation towards and away from the lesioned side, respectively. The optokinetic beating field was similarly deviated. Under these experimental conditions, HVOR showed enhanced gain and marked misalignment in both eyes. Therefore, the selective suppression of muscular proprioceptive input deviated both eyes towards the direction opposite to the muscle whose gangliar proprioceptive representation has been destroyed.

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

The mammalian oculomotor nucleus receives a strong γ-aminobutyric acid (GABA)ergic synaptic input, whereas such projections have rarely been reported in fish. In order to determine whether this synaptic organization is preserved across vertebrates, we investigated the GABAergic projections to the oculomotor nucleus in the goldfish by combining retrograde transport of biotin dextran amine, injected into the antidromically identified oculomotor nucleus, and GABA immunohistochemistry.The main source of GABAergic afferents to the oculomotor nucleus was the ipsilateral anterior octaval nucleus, with only a few, if any, GABAergic neurons being located in the contralateral tangential and descending nuclei of the octaval column. In mammals there is a nearly exclusive ipsilateral projection from vestibular neurons to the oculomotor nucleus via GABAergic inhibitory inputs; thus, the vestibulooculomotor GABAergic circuitry follows a plan that appears to be shared throughout the vertebrate phylogeny. The second major source of GABAergic projections was the rhombencephalic reticular formation, primarily from the medial area but, to a lesser extent, from the inferior area. A few GABAergic oculomotor projecting neurons were also observed in the ipsilateral nucleus of the medial longitudinal fasciculus. The GABAergic projections from neurons located in both the reticular formation surrounding the abducens nucleus and the nucleus of the medial reticular formation have primarily been related to the control of saccadic eye movements. Finally, all retrogradely labeled internuclear neurons of the abducens nucleus, and neurons in the cerebellum (close to the caudal lobe), were negative for GABA. These data suggest that the vestibuloocular and saccadic inhibitory GABAergic systems appear early in vertebrate phylogeny to modulate the firing properties of the oculomotor nucleus motoneurons. Ministerio de Innovación y Ciencia BFU 2009-07867 Junta de Andalucía P08-CVI-039 y P09-CVI-4617

Prolonged exposure to hypergravity in a human centrifuge can lead to post-rotary spatial disorientation and motion sickness. These symptoms are mainly provoked by tilting head movements and resemble the Space Adaptation Syndrome. We hypothesized that the occurrence of these post-rotary effects might be related to changes in the velocity storage (VS) mechanism, which is suggested to play an important role in spatial orientation. In particular, we investigated whether the re-orientation of the eye velocity vector (EVV) towards gravity during off-vertical optokinetic stimulation was affected by centrifugation. Twelve human subjects were exposed to a hypergravity load of 3G (G-load directed along the naso-occipetal axis) for a duration of 90 min. Before and after centrifugation we recorded optokinetic nystagmus (OKN) elicited by a stimulus pattern moving about the subject’s yaw axis, with the head erect and tilted 45 to both sides. During OKN with the head erect, we observed a pitch-down component, reorienting the EVV on average 4.5 (SD 3.6, pretest values) away from the stimulus axis. Head tilt induced an additional shift of the EVV towards the spatial vertical of 6.4 on average (SD 3.2). This head-tilt induced reorientation was significantly decreased after centrifugation to 4.7 (SD 2.9), suggesting a reduction of VS-activity. By means of a vector model we estimated the reduction in VSactivity at 31%. Such a decrease in VS-activity light reflect a deterioration of the ability to integrate sensory signals to obtain an estimate of gravity during tilting head movements, resulting in motion sickness in susceptible subjects. Keywords Hypergravity, Optokinetic nystagmus, Vestibular adaptation, Human, Motion sickness, Gravity

We tested the hypothesis that the importance of calf muscle-tendon properties for maintaining balance during single-leg stance increases in the absence of visual feedback. Trial duration, centre of pressure displacement normalized for trial duration (nD), electromyographic (EMG) activity of the main ankle plantarflexors and dorsiflexors, and ground reaction forces (F(P)), were measured in 20 younger (aged 18+/-1 years; mean+/-S.E.M.) and 28 older (aged 68+/-1 years) healthy participants during single-leg stance in eyes-open (EO) and eyes-closed (EC) conditions. Plantarflexor muscle strength, activation capacity and tendon stiffness were assessed by dynamometry, electrical stimulation and ultrasonography, respectively. Muscle-tendon characteristics in the older participants were up to 55% (P0.0001) lower compared with their younger counterparts. Trial duration, F(P), nD and EMG changed in EC compared with EO by 21% and up to approximately 4.6 times (P0.01) in the two population groups. Multiple linear regression with age and the three muscle-tendon properties showed a substantial increment in EC compared to EO for trial duration (R(2)=0.86 versus R(2)=0.72), but a similarity for nD (R(2)=0.36 versus R(2)=0.33). These results suggest that factors other than the ones that we examined become important when steadiness rather than stance duration is the object of single-leg stance in the absence of vision.

Immersion in an illusory world is possible by means of virtual reality (VR), where environmental perception is modified by artificial sensorial stimulation. The application of VR for the assessment and rehabilitation of pathologies affecting the vestibular system, in terms of both diagnosis and care, could represent an interesting new line of research. Our perception of reality is in fact based on static and dynamic spatial information perceived by our senses. During head movements in a virtual environment the images on the display and the labyrinthine information relative to the head angular accelerations differ and therefore a visuo-vestibular conflict is present. It is known that mismatches between visual and labyrinthine information may modify the vestibulo-oculomotor reflex (VOR) gain. We studied the post-immersion modifications in 20 healthy subjects (mean age 25 years) exposed to a virtual environment for 20 min by wearing a head-mounted display. VOR gain and phase were measured by means of harmonic sinusoidal stimulation in the dark before, at the end of and 30 min after VR exposure. A VOR gain reduction was observed in all subjects at the end of VR exposure which disappeared after 30 min. Our data show that exposure to a virtual environment can induce a temporary modification of the VOR gain. This finding can be employed to enable an artificial, instrumental modification of the VOR gain and therefore opens up new perspectives in the assessment and rehabilitation of vestibular diseases.

Item does not contain fulltext It is still debated to what extent the vestibular deficits in Usher patients are due to either central vestibulocerebellar or peripheral vestibular problems. Here, we determined the origin of the vestibular symptoms in Usher 1B patients by subjecting them to compensatory eye movement tests and by investigating the shaker-1 mouse model, which is known to have the same mutation in the myosin-VIIa gene as Usher 1B patients. We show that myosin-VIIa is not expressed in the human or mouse cerebellum and that the vestibulocerebellum of both Usher 1B patients and shaker-1 mice is functionally intact in that the gain and phase values of their optokinetic reflex are normal. In addition, Usher 1B patients and shaker-1 mice do not show an angular vestibuloocular reflex even though eye movement responses evoked by electrical stimulation of the vestibular nerve appear intact. Finally, we show histological abnormalities in the vestibular hair cells of shaker-1 mice at the ultrastructural level, while the distribution of the primary vestibular afferents and the vestibular brainstem circuitries are unaffected. We conclude that the vestibular dysfunction of Usher 1B patients and shaker-1 mice is peripheral in origin.

Little is known about the vestibulo-perceptual (VP) system, particularly after a unilateral vestibular lesion. We investigated vestibulo-ocular (VO) and VP function in 25 patients with vestibular neuritis (VN) acutely (2 days after onset) and after compensation (recovery phase, 10 weeks). Since the effect of VN on reflex and perceptual function may differ at threshold and supra-threshold acceleration levels, we used two stimulus intensities, acceleration steps of 0.5°/s(2) and velocity steps of 90°/s (acceleration 180°/s(2)). We hypothesised that the vestibular lesion or the compensatory processes could dissociate VO and VP function, particularly if the acute vertiginous sensation interferes with the perceptual tasks. Both in acute and recovery phases, VO and VP thresholds increased, particularly during ipsilesional rotations. In signal detection theory this indicates that signals from the healthy and affected side are still fused, but result in asymmetric thresholds due to a lesion-induced bias. The normal pattern whereby VP thresholds are higher than VO thresholds was preserved, indicating that any 'perceptual noise' added by the vertigo does not disrupt the cognitive decision-making processes inherent to the perceptual task. Overall, the parallel findings in VO and VP thresholds imply little or no additional cortical processing and suggest that vestibular thresholds essentially reflect the sensitivity of the fused peripheral receptors. In contrast, a significant VO-VP dissociation for supra-threshold stimuli was found. Acutely, time constants and duration of the VO and VP responses were reduced - asymmetrically for VO, as expected, but surprisingly symmetrical for perception. At recovery, VP responses normalised but VO responses remained shortened and asymmetric. Thus, unlike threshold data, supra-threshold responses show considerable VO-VP dissociation indicative of additional, higher-order processing of vestibular signals. We provide evidence of perceptual processes (ultimately cortical) participating in vestibular compensation, suppressing asymmetry acutely in unilateral vestibular lesions.

The contribution of the maculo-ocular reflex to gaze stability was studied in 10 pigmented rabbits by rolling the animals at various angles of sagittal inclination of the rotation and/or longitudinal animal axes. At low frequencies (0.005–0.01 Hz) of sinusoidal stimulation the vestibulo-ocular reflex (VOR) was due to macular activation, while at intermediate and high frequencies it was mainly due to ampullar activation. The following results were obtained: 1) maculo-ocular reflex gain decreased as a function of the cosine of the angle between the rotation axis and the earth's horizontal plane. No change in gain was observed when longitudinal animal axis alone was inclined. 2) At 0° of rotation axis and with the animal's longitudinal axis inclination also set at 0°, the maculo-ocular reflex was oriented about 20° forward and upward with respect to the earth's vertical axis. This orientation remained constant with sagittal inclinations of the rotation and/or longitudinal animal axes ranging from approximately 5° upward to 30° downward. When the longitudinal animal axis was inclined beyond these limits, the eye trajectory tended to follow the axis inclination. In the upside down position, the maculo-ocular reflex was anticompensatory, oblique and fixed with respect to orbital coordinates. 3) Ampullo-ocular reflex gain did not change with inclinations of the rotation and/or longitudinal animal axes. The ocular responses were consistently oriented to the stimulus plane. At intermediate frequencies the eye movement trajectory was elliptic because of directional differences between the ampullo- and maculo-ocular reflexes. 4) In the upright position the coactivation of the optokinetic reflex (OKR) eliminated the eye disalignment with respect to the stimulus plane and the elliptic trajectory. 5) Combined vertical OKR and VOR gain in the prone position (VOKR + VVOR 0°) was higher than that of the combined VOKR + VVOR in the 90° nose up position. The VVOR + VOKR 90° gain was in turn higher than the VVOR + VOKR gain in the 180° upside down position. 6) We suggest that, in the dark, the maculo-ocular response tends to reduce the disalignment of both eyes with respect to the horizon rather than inducing oculocompensatory responses. In the light, this maculo-ocular reflex increases the gain of combined optokinetic and vestibular responses.