Passive Head Movements Research Articles

Are Vestibuloocular Reflex Gain and Dynamic Visual Acuity Responsible of Oscillopsia After Complete Unilateral Vestibular Loss?

Acute and complete unilateral vestibular deafferentation induces a significant change in ipsilateral vestibuloocular reflex gain, making the patient unable to stabilize gaze during active or passive head movements. This inability creates the illusion that the visual environment is moving, resulting in persistent visual discomfort during rapid angular or linear acceleration of the head. This is known as oscillopsia. Our objective was to understand if the spontaneous sensation of oscillopsias after complete unilateral vestibular deafferentation by vestibular neurotomy at 5 days (D5) and at 3 months (M3) is correlated with the loss of vestibuloocular reflex gain and dynamic visual acuity. Retrospective cohort study was conducted in an otolaryngology tertiary care center (2019-2022) on patients with complete unilateral vestibular loss by vestibular neurotomy. They were divided into 2 groups according to the presence (group G1) or absence (group G2) of a spontaneous complaint of oscillopsia assessed at M3. Severity of oscillopsias evaluated by Oscillopsia Severity Questionnaire. Vestibuloocular reflex gain based on video head impulse test (vHIT) and the dynamic visual acuity were measured for each group at D5 and M3. Categorical variables were compared using χ2 test and quantitative variables using the nonparametric Wilcoxon-Mann-Whitney test. All patients have a complete vestibular deafferentation at D5 and M3. At D5 (G1 = 8 patients, G2 = 5 patients), there is no significant difference for ipsilateral and contralateral vestibuloocular reflex gains and dynamic visual acuity losses. The Oscillopsia Severity Questionnaire was 2.68 ± 1.03 in G1 and 1.23 ± 1.03 in G2 (P < .05). At M3 (G1 = 9 patients, G2 = 6 patients), there is no significant difference between groups for epidemiologic and clinical data and for vestibuloocular reflex and dynamic visual acuity losses. The Oscillopsia Severity Questionnaire was 2.10 ± 0.63 in G1 and 1.24 ± 0.28 in G2 (P < .05). The spontaneous disabling sensation of oscillopsia after complete unilateral vestibular loss is well assessed by the Oscillopsia Severity Questionnaire but cannot be explained by objective vestibular tests assessing vestibuloocular reflex gain (vHIT) or dynamic visual acuity loss at D5 or M3. Further studies are needed to measure the sensation of oscillopsia under real-life conditions and to identify the factors responsible for its persistence. Retrospectively registered.

Changes in vestibular-related responses to combined noisy galvanic vestibular stimulation and cerebellar transcranial direct current stimulation.

Vestibular nuclei and cerebellar function comprise vestibular neural networks that control vestibular-related responses. However, the vestibular-related responses to simultaneous stimulation of these regions are unclear. This study aimed to examine whether the combination of noisy galvanic vestibular stimulation (nGVS) and cerebellar transcranial direct current stimulation (ctDCS) using a complex transcranial electrical stimulation device alters vestibular-dominant standing stability and vestibulo-ocular reflex (VOR) function. The center of foot pressure (COP) sway and VOR of participants (28 healthy, young adults) were assessed under four conditions of transcranial electrical stimulation using nGVS and ctDCS. The COP was calculated with the participant standing on a soft-foam surface with eyes closed using a force plate to evaluate body sway. VOR measurements were collected via passive head movements and fixation on a target projected onto the front wall using a video head impulse test (vHIT). VOR gain was calculated in six directions using a semicircular canal structure based on the ratio of eye movement to head movement. The nGVS + ctDCS and nGVS + sham ctDCS conditions decreased COP sway compared to the sham nGVS + ctDCS and sham nGVS + sham ctDCS conditions. No significant differences were observed in the main effect of stimulation or the interaction of stimulation and direction on the vHIT parameters. The results of this study suggest that postural stability may be independently affected by nGVS. Our findings contribute to the basic neurological foundation for the clinical application of neurorehabilitation using transcranial electrical stimulation of the vestibular system.

Motor Signals Mediate Stationarity Perception.

Head movement relative to the stationary environment gives rise to congruent vestibular and visual optic-flow signals. The resulting perception of a stationary visual environment, referred to herein as stationarity perception, depends on mechanisms that compare visual and vestibular signals to evaluate their congruence. Here we investigate the functioning of these mechanisms and their dependence on fixation behavior as well as on the active versus passive nature of the head movement. Stationarity perception was measured by modifying the gain on visual motion relative to head movement on individual trials and asking subjects to report whether the gain was too low or too high. Fitting a psychometric function to the data yields two key parameters of performance. The mean is a measure of accuracy, and the standard deviation is a measure of precision. Experiments were conducted using a head-mounted display with fixation behavior monitored by an embedded eye tracker. During active conditions, subjects rotated their heads in yaw ∼15deg/s over ∼1s. Each subject's movements were recorded and played back via rotating chair during the passive condition. During head-fixed and scene-fixed fixation the fixation target moved with the head or scene, respectively. Both precision and accuracy were better during active than passive head movement, likely due to increased precision on the head movement estimate arising from motor prediction and neck proprioception. Performance was also better during scene-fixed than head-fixed fixation, perhaps due to decreased velocity of retinal image motion and increased precision on the retinal image motion estimate. These results reveal how the nature of head and eye movements mediate encoding, processing, and comparison of relevant sensory and motor signals.

PS-B07-1: BRAIN-TARGETED MECHANICAL INTERVENTION USING PASSIVE HEAD MOTION CAN BE ANTIHYPERTENSIVE

Objective: Reproduce the antihypertensive effect of physical exercise by applying mechanical intervention. Design and method: We conducted animal experiments in which we reproduced mechanical accelerations generated in the head during treadmill running at a moderate velocity. We performed in vitro experiments using cultured cells to determine what type of mechanical force was responsible for the antihypertensive effect of mechanical intervention. We carried out clinical studies to validate the clinical relevance of our findings. Results: Passive head motion in hypertensive rats, which reproduced the mechanical accelerations generated in their heads during treadmill running at a moderate velocity, decreased the expression of angiotensin II type 1 receptor (AT1R) in astrocytes in the rostral ventrolateral medulla (RVLM). This decrease resulted in lowering their blood pressure. Passive head motion generated interstitial fluid movement, which was estimated to exert shearing forces with an average magnitude of &lt; 1 Pa on the cells in the rat medulla. Application of fluid shear stress of relevant magnitudes decreased the AT1R expression in cultured astrocytes, but not in neuronal cells. Furthermore, interference with interstitial fluid movement by hydrogel introduction in the RVLM of hypertensive rats eliminated the ability of passive head motion and treadmill running to decrease their blood pressure and AT1R expression in the RVLM astrocytes. Consistent with these results from animal experiments, vertically oscillating chair riding by hypertensive adult humans, which reproduced the mechanical accelerations generated in their heads during light jogging, lowered their blood pressure. Conclusion: Brain-targeted mechanical intervention can be antihypertensive by modulating the function of RVLM astrocytes through interstitial fluid shear stress.

Abstract 9243: Brain-Targeted Mechanical Intervention Using Passive Head Motion Can Have an Antihypertensive Effect

Introduction: Exercise is known to be effective as a therapeutic/preventative measure for numerous physical disorders and diseases including hypertension. However, the mechanisms underlying the antihypertensive effect of exercise remain to be elucidated. Hypothesis: The positive effects of exercise may be mediated by mechanical forces generated during exercise activities. Exercise-mimicking mechanical intervention may have an antihypertensive effect. Methods: We conducted animal experiments in which we reproduced mechanical accelerations generated in the head during moderate-velocity running. We performed in vitro experiments using cultured cells to determine what type of mechanical force was responsible for the antihypertensive effect of mechanical intervention. We carried out clinical studies to validate the clinical relevance of our findings. Results: Passive head motion (PHM) in hypertensive rats, which reproduced the mechanical accelerations generated in their heads during moderate-velocity treadmill running, decreased the expression of angiotensin II type 1 receptor (AT1R) in astrocytes in the rostral ventrolateral medulla (RVLM), thereby lowering their blood pressure. PHM generated interstitial fluid movement that was estimated to exert shear stress with an average magnitude of &lt;1 Pa on the cells in the rat medulla. Fluid shear stress of a sub-Pa magnitude decreased the AT1R expression in cultured astrocytes. Inhibition of interstitial fluid movement following hydrogel introduction to the RVLM eliminated the antihypertensive effects of PHM and treadmill running. Vertically oscillating chair riding by hypertensive adult humans, which reproduced the mechanical accelerations generated in their heads during light jogging, lowered their blood pressure. Conclusion: Brain-targeted mechanical intervention can have an antihypertensive effect by modulating the function of RVLM astrocytes through interstitial fluid shear stress.

Application of Passive Head Motion to Generate Defined Accelerations at the Heads of Rodents.

Exercise is widely recognized as effective for various diseases and physical disorders, including those related to brain dysfunction. However, molecular mechanisms behind the beneficial effects of exercise are poorly understood. Many physical workouts, particularly those classified as aerobic exercises such as jogging and walking, produce impulsive forces at the time of foot contact with the ground. Therefore, it was speculated that mechanical impact might be implicated in how exercise contributes to organismal homeostasis. For testing this hypothesis on the brain, a custom-designed ''passive head motion'' (hereafter referred to as PHM) system was developed that can generate vertical accelerations with controlled and defined magnitudes and modes and reproduce mechanical stimulation that might be applied to the heads of rodents during treadmill running at moderate velocities, a typical intervention to test the effects of exercise in animals. By using this system, it was demonstrated that PHM recapitulates the serotonin (5-hydroxytryptamine, hereafter referred to as 5-HT) receptor subtype 2A (5-HT2A) signaling in the prefrontal cortex (PFC) neurons of mice. This work provides detailed protocols for applying PHM and measuring its resultant mechanical accelerations at rodents' heads.

Application of Passive Head Motion to Generate Defined Accelerations at the Heads of Rodents

Application of Passive Head Motion to Generate Defined Accelerations at the Heads of Rodents

Influence of predictability on saccade timing in a head impulse VOR suppression task.

Gaze stabilization performance has been shown to be influenced differently when the head is either passively or actively moved in normal healthy participants. However, for a visual fixation suppression task, it remains unknown if the pattern of coordinated head and eye movement is influenced differently by passive or active head movements. We used a suppression head impulse paradigm (SHIMP), where the subject's goal was to maintain gaze stabilized on a visual target that moved with the head during rapid impulsive head movements, to evaluate gaze fixation performance in three conditions: (1) passive-unpredictable where the examiner applied impulsive head yaw rotations with random timing and direction, (2) passive-predictable where the direction of head rotation was announced and then the examiner repeatedly applied impulses in the same direction, and (3) active where the test subject self-generated their head movements. Thirteen young healthy adults performed all three conditions to assess the percentage of early saccades that initiated the gaze shift toward the final visual target position and the latency of first saccades. Early saccades were defined as those occurring within the duration of the head impulse. Results showed that active head impulses generated the greatest percentage of early saccades, followed by predictable and unpredictable. Among the two passive conditions, predictability shortened the first saccade onset latencies. Active condition onset latencies were shorter than in either of the passive conditions, showing a consistent head-leads-eye pattern defining a specific behavioral pattern that could vary across patient groups leading to insights into central neural mechanisms that control eye-head coordination.

The Effect of Different Head Movement Paradigms on Vestibulo-Ocular Reflex Gain and Saccadic Eye Responses in the Suppression Head Impulse Test in Healthy Adult Volunteers.

Objective: This study aimed to identify differences in vestibulo-ocular reflex gain (VOR gain) and saccadic response in the suppression head impulse paradigm (SHIMP) between predictable and less predictable head movements, in a group of healthy subjects. It was hypothesized that higher prediction could lead to a lower VOR gain, a shorter saccadic latency, and higher grouping of saccades.Methods: Sixty-two healthy subjects were tested using the video head impulse test and SHIMPs in four conditions: active and passive head movements for both inward and outward directions. VOR gain, latency of the first saccade, and the level of saccade grouping (PR-score) were compared among conditions. Inward and active head movements were considered to be more predictable than outward and passive head movements.Results: After validation, results of 57 tested subjects were analyzed. Mean VOR gain was significantly lower for inward passive compared with outward passive head impulses (p < 0.001), and it was higher for active compared with passive head impulses (both inward and outward) (p ≤ 0.024). Mean latency of the first saccade was significantly shorter for inward active compared with inward passive (p ≤ 0.001) and for inward passive compared with outward passive head impulses (p = 0.012). Mean PR-score was only significantly higher in active outward than in active inward head impulses (p = 0.004).Conclusion: For SHIMP, a higher predictability in head movements lowered gain only in passive impulses and shortened latencies of compensatory saccades overall. For active impulses, gain calculation was affected by short-latency compensatory saccades, hindering reliable comparison with gains of passive impulses. Predictability did not substantially influence grouping of compensatory saccades.

Short-Latency Covert Saccades - The Explanation for Good Dynamic Visual Performance After Unilateral Vestibular Loss?

Background: Functional head impulse test (fHIT) tests the ability of the vestibulo-ocular reflex (VOR) to allow visual perception during head movements. Our previous study showed that active head movements to the side with a vestibular lesion generated a dynamic visual performance that were as good as during movements to the intact side.Objective: To examine the differences in eye position during the head impulse test when performed with active and passive head movements, in order to better understand the role of the different saccade properties in improving visual performance.Method: We recruited 8 subjects with complete unilateral vestibular loss (4 men and 4 women, mean age 47 years) and tested them with video Head Impulse Test (vHIT) and Functional Head Impulse Test (fHIT) during passive and active movements while looking at a target. We assessed the mean absolute position error of the eye during different time frames of the head movement, the peak latency and the peak velocity of the first saccade, as well as the visual performance during the head movement.Results: Active head impulses to the lesioned side generated dynamic visual performances that were as good as when testing the intact side. Active head impulses resulted in smaller position errors during the visual perception task (p = 0.006) compared to passive head-impulses and the position error during the visual perception time frame correlated with shorter latencies of the first saccade (p < 0.001).Conclusion: Actively generated head impulses toward the side with a complete vestibular loss resulted in a position error within or close to the margin necessary to obtain visual perception for a brief period of time in patients with chronic unilateral vestibular loss. This seems to be attributed to the appearance of short-latency covert saccades, which position the eyes in a more favorable position during head movements.

The morphology, biomechanics, and physiological function of the suboccipital myodural connections

The myodural bridge (MDB) connects the suboccipital musculature to the spinal dura mater (SDM) as it passed through the posterior atlanto-occipital and the atlanto-axial interspaces. Although the actual function of the MDB is not understood at this time, it has recently been proposed that head movement may assist in powering the movement of cerebrospinal fluid (CSF) via muscular tension transmitted to the SDM via the MDB. But there is little information about it. The present study utilized dogs as the experimental model to explore the MDB’s effects on the CSF pressure (CSFP) during stimulated contractions of the suboccipital muscles as well as during manipulated movements of the atlanto-occiptal and atlanto-axial joints. The morphology of MDB was investigated by gross anatomic dissection and by histological observation utilizing both light microscopy and scanning electron microscopy. Additionally biomechanical tensile strength tests were conducted. Functionally, the CSFP was analyzed during passive head movements and electrical stimulation of the suboccipital muscles, respectively. The MDB was observed passing through both the dorsal atlanto-occipital and the atlanto-axial interspaces of the canine and consisted of collagenous fibers. The tensile strength of the collagenous fibers passing through the dorsal atlanto-occipital and atlanto-axial interspaces were 0.16 ± 0.04 MPa and 0.82 ± 0.57 MPa, respectively. Passive head movement, including lateral flexion, rotation, as well as flexion–extension, all significantly increased CSFP. Furthermore, the CSFP was significantly raised from 12.41 ± 4.58 to 13.45 ± 5.16 mmHg when the obliques capitis inferior (OCI) muscles of the examined specimens were electrically stimulated. This stimulatory effect was completely eliminated by severing the myodural bridge attachments to the OCI muscle. Head movements appeared to be an important factor affecting CSF pressure, with the MDB of the suboccipital muscles playing a key role this process. The present study provides direct evidence to support the hypothesis that the MDB may be a previously unappreciated significant power source (pump) for CSF circulation.

Functional organization of vestibulospinal inputs on thoracic motoneurons responsible for trunk postural control in Xenopus.

Vestibulospinal reflexes participate in postural control. How this is achieved has not been investigated fully. We combined electrophysiological, neuroanatomical and imaging techniques to decipher the vestibulospinal network controlling the activation of back and limb muscles responsible for postural adjustments. We describe two distinct pathways activating either thoracic postural motoneurons alone or thoracic and lumbar motoneurons together, with the latter co-ordinating specifically hindlimb extensors and postural back muscles. In vertebrates, trunk postural stabilization is known to rely mainly on direct vestibulospinal inputs on spinal axial motoneurons. However, a substantial role of central spinal commands ascending from lumbar segments is not excluded during active locomotion. In the adult Xenopus, a lumbar drive dramatically overwhelms the descending inputs onto thoracic postural motoneurons during swimming. Given that vestibulospinal fibres also project onto the lumbar segments that shelter the locomotor generators, we investigated whether such a lumbo-thoracic pathway may relay vestibular information and consequently, also be involved in the control of posture at rest. We show that thoracic postural motoneurons exhibit particular dendritic spatial organization allowing them to gather information from both sides of the cord. In response to passive head motion, these motoneurons display both early and delayed discharges, with the latter occurring in phase with ipsilateral hindlimb extensor bursts. We demonstrate that both vestibulospinal and lumbar ascending fibres converge onto postural motoneurons, and that thoracic motoneurons monosynaptically respond to the electrical stimulation of either pathway. Finally, we show that vestibulospinal fibres project to and activate lumbar interneurons with thoracic projections. Taken together, our results complete the scheme of the vestibulospinal control of posture by illustrating the existence of a novel, indirect pathway, which implicates lumbar interneurons relaying vestibular inputs to thoracic motoneurons, and participating in global body postural stabilization in the absence of active locomotion.

Mechanical Regulation Underlies Effects of Exercise on Serotonin-Induced Signaling in the Prefrontal Cortex Neurons.

SummaryMechanical forces are known to be involved in various biological processes. However, it remains unclear whether brain functions are mechanically regulated under physiological conditions. Here, we demonstrate that treadmill running and passive head motion (PHM), both of which produce mechanical impact on the head, have similar effects on the hallucinogenic 5-hydroxytryptamine (5-HT) receptor subtype 2A (5-HT2A) signaling in the prefrontal cortex (PFC) of rodents. PHM generates interstitial fluid movement that is estimated to exert shear stress of a few pascals on cells in the PFC. Fluid shear stress of a relevant magnitude on cultured neuronal cells induces ligand-independent internalization of 5-HT2A receptor, which is observed in mouse PFC neurons after treadmill running or PHM. Furthermore, inhibition of interstitial fluid movement by introducing polyethylene glycol hydrogel eliminates the effect of PHM on 5-HT2A receptor signaling in the PFC. Our findings indicate that neuronal cell function can be physiologically regulated by mechanical forces in the brain.

Effects of Passive Head-and-Neck Movements on the Performance of i-gel® Supraglottic Airway Device in Anesthetized Patients - A Randomized Crossover Trial.

Background:Passive movements of head and neck are sometimes unavoidable during surgery under general anesthesia due to patient positioning according to the needs of the surgery or transmitted movements from surgical manipulations.Aims:This prospective crossover randomized study evaluates the effects of passive movements of the head and neck on the performance of i-gel® supraglottic airway device in spontaneously breathing patients under general anesthesia.Materials and Methods:Sixty spontaneously breathing patients on pressure support ventilation with positive end-expiratory pressure (PEEP) under general anesthesia were randomized to seven sequences of passive head-and-neck movements with i-gel® in situ. After steady state of general anesthesia was achieved and maintenance with sevoflurane in N2O and O2 was reached, the passive head-and-neck movements were done. Peak airway pressure, exhaled minute volume, end-tidal carbon dioxide (ETCO2), oxygen saturation, audible leak of airway gases, and visible outward displacement of the i-gel® were recorded in the neutral position and with each passive head-and-neck movement. Paired continuous data were analyzed by Friedman rank sum test with paired Wilcoxon signed-rank test. Paired nominal data were analyzed by Cochran's Q test with pair-wise McNemar test.Results:Extension, right or left lateral flexion, and right or left rotation of the head and neck resulted in significant reduction in the exhaled minute ventilation, rise in ETCO2, and leak of airway gases compared to the neutral position (P < 0.05). Flexion movement did not cause significant changes in the exhaled minute ventilation, rise in ETCO2, and audible leak of airway gases as compared to the neutral position.Conclusions:Ventilatory performance of the i-gel® deteriorates upon extension, right or left lateral flexion, and right or left rotation of the head and neck in spontaneously breathing patients under general anesthesia on pressure support ventilation with PEEP.

Towards a ‘Green Allopathy’: Biomedicalization and the Naturopathic Medicine Profession in Ontario, Canada

Different classes of primary afferents from semicircular canal and otolith organs project to the vestibular nuclei, but do not follow a topographic representation as seen for other sense organs. Second-order vestibular neurons give rise to different pathways that serve gaze and body stabilization during active and passive head motion or self-motion perception and spatial orientation. These projections originate in specific genetically determined hindbrain segments and are defined by their motor or premotor targets, an organization that appears to be preserved throughout vertebrate evolution.

Functional Head Impulse Testing Might Be Useful for Assessing Vestibular Compensation After Unilateral Vestibular Loss.

Background: Loss of the vestibulo-ocular reflex (VOR) affects visual acuity during head movements. Previous studies have shown that compensatory eye-saccades improve visual acuity and that the timing of the saccade is important. Most of the tests involved in testing VOR are made with passive head movement, that do not necessarily reflect the activities of daily living and thus not being proportionate to symptoms and distresses of the patients.Objective: To examine differences between active (self-generated) or passive (imposed by the examiner) head rotations while trying to maintain visual focus on a target.Method: Nine subjects with unilateral total vestibular loss were recruited (4 men and 5 women, mean age 47) and tested with video Head Impulse Test (vHIT) and Head Impulse Testing Device-Functional Test (HITD-FT) during passive and active movements while looking at a target. VOR gain, latencies of covert saccades, frequency of covert saccades and visual acuity were measured and analyzed.Results: Active head-impulses toward the lesioned side resulted in better visual acuity (p = 0.002) compared to conventional passive head-impulses and generated eye-saccades with significantly shorter latencies (p = 0.004). Active movements to the lesioned side generated dynamic visual acuities that were as good as when testing the intact side.Conclusion: Actively generated head impulses resulted in normal dynamic visual acuity, even when performed toward the side of total vestibular loss. This might be attributed to the appearance of short-latency covert saccades. The results show a strong relationship between self-generated movements, latencies of covert saccades and outcome in HITD-FT, i.e., a better dynamic visual function with less retinal slip which is the main function of the VOR. The method of active HITD-FT might be valuable in assessing vestibular compensation and monitoring ongoing vestibular rehabilitation.

A virtual reality approach identifies flexible inhibition of motion aftereffects induced by head rotation.

As we move in space, our retinae receive motion signals from two causes: those resulting from motion in the world and those resulting from self-motion. Mounting evidence has shown that vestibular self-motion signals interact with visual motion processing profoundly. However, most contemporary methods arguably lack portability and generality and are incapable of providing measurements during locomotion. Here we developed a virtual reality approach, combining a three-space sensor with a head-mounted display, to quantitatively manipulate the causality between retinal motion and head rotations in the yaw plane. Using this system, we explored how self-motion affected visual motion perception, particularly the motion aftereffect (MAE). Subjects watched gratings presented on a head-mounted display. The gratings drifted at the same velocity as head rotations, with the drifting direction being identical, opposite, or perpendicular to the direction of head rotations. We found that MAE lasted a significantly shorter time when subjects' heads rotated than when their heads were kept still. This effect was present regardless of the drifting direction of the gratings, and was also observed during passive head rotations. These findings suggest that the adaptation to retinal motion is suppressed by head rotations. Because the suppression was also found during passive head movements, it should result from visual-vestibular interaction rather than from efference copy signals. Such visual-vestibular interaction is more flexible than has previously been thought, since the suppression could be observed even when the retinal motion direction was perpendicular to head rotations. Our work suggests that a virtual reality approach can be applied to various studies of multisensory integration and interaction.

Head-Movement-Emphasized Rehabilitation in Bilateral Vestibulopathy.

Objective: Although there is evidence that vestibular rehabilitation is useful for treating chronic bilateral vestibular hypofunction (BVH), the mechanisms for improvement, and the reasons why only some patients improve are still unclear. Clinical rehabilitation results and evidence fromeye-head control in vestibular deficiency suggest that headmovement is a crucial element of vestibular rehabilitation. In this study, we assess the effects of a specifically designed head-movement-based rehabilitation program on dynamic vision, and explore underlying mechanisms.Methods: Two adult patients (patients 1 and 2) with chronic BVH underwent two 4-week interventions: (1) head-movement-emphasized rehabilitation (HME) with exercises based on active head movements, and (2) eye-movement-only rehabilitation (EMO), a control intervention with sham exercises without head movement. In a double-blind crossover design, the patients were randomized to first undergo EMO (patient 1) and–after a 4-week washout–HME, and vice-versa (patient 2). Before each intervention and after a 4-week follow-up patients’ dynamic vision, vestibulo-ocular reflex (VOR) gain, as well as re-fixation saccade behavior during passive headmotion were assessed with the head impulse testing device–functional test (HITD-FT).Results: HME, not EMO, markedly improved perception with dynamic vision during passive head motion (HITD-FT score) increasing from 0 to 60% (patient 1) and 75% (patient 2). There was a combination of enhanced VOR, as well as improved saccadic compensation.Conclusion: Head movement seems to be an important element of rehabilitation for BVH. It improves dynamic vision with a combined VOR and compensatory saccade enhancement.

The Interaction of Pre-programmed Eye Movements With the Vestibulo-Ocular Reflex.

The Vestibulo-Ocular Reflex (VOR) works to stabilize gaze during unexpected head movements. However, even subjects who lack a VOR (e.g., vestibulopathic patients) can achieve gaze stability during planned head movements by using pre-programmed eye movements (PPEM). The extent to which PPEM are used by healthy intact subjects and how they interact with the VOR is still unclear. We propose a model of gaze stabilization which makes several claims: (1) the VOR provides ocular stability during unexpected (i.e., passive) head movements; (2) PPEM are used by both healthy and vestibulopathic subjects during planned (i.e., active) head movements; and (3) when a passive perturbation interrupts an active head movement in intact animals (i.e., combined passive and active head movement) the VOR works with PPEM to provide compensation. First, we show how our model can reconcile some seemingly conflicting findings in earlier literature. We then test the above-mentioned predictions against data we collected from both healthy and vestibular-lesioned guinea pigs. We found that (1) vestibular-lesioned animals showed a dramatic decrease in compensatory eye movements during passive head movements, (2) both populations showed improved ocular compensation during active vs. passive head movements, and (3) during combined active and passive head movements, eye movements compensated for both the active and passive component of head velocity. These results support our hypothesis that while the VOR provides compensation during passive head movements, PPEM are used by both intact and lesioned subjects during active movements and further, that PPEM work together with the VOR to achieve gaze stability.

The head impulse test as a predictor of videonystagmography caloric test lateralization according to the level of examiner experience: A prospective open-label study.

We conducted a study to compare how well the head impulse test (HIT), without and with eye-movement recordings, would predict videonystagmographic (VNG) caloric test lateralization when performed by a resident and an experienced otoneurologist. This prospective, open-label, blinded study was conducted in an ambulatory tertiary care referral center. Our study population was made up of 60 patients-29 men and 31 women, aged 20 to 82 years (mean: 56.4 ± 11.4)-with peripheral vestibulopathy who underwent HIT and VNG caloric testing. The HIT was conducted in two protocols: HIT0 and HIT1. The HIT0 was performed with passive brisk movements of the patient's head from the 0° null position to 20° sideways, and the HIT1 was performed toward the center while the null position was a 20° head rotation to the right and to the left. Each protocol was carried out without video eye-movement recordings (HIT0 and HIT1) and with such recordings (rHIT0 and rHIT1). The primary outcome measures were (1) a comparison of the HIT's sensitivity and specificity when performed by the resident and by the experienced otoneurologist and (2) the ability of video-recorded HIT to predict VNG caloric test lateralization. The sensitivity and specificity obtained by the resident were 41 and 81%, respectively, for HIT0 and 41 and 90% for HIT1. The sensitivity and specificity obtained by the experienced otoneurologist were 18 and 89% for HIT0 and 32 and 85% for HIT1. Analysis of the recorded eye-movement clips of the HIT0 and HIT1 obtained by a second experienced otoneurologist found a sensitivity and specificity of 32 and 63% for rHIT0 and 33 and 82% for rHIT1. We conclude that the HIT yields high false-negative rates in predicting significant caloric lateralization. Analysis of the eye-movement recordings was no better than normal testing alone for detecting saccades. The experience of the examining physician had no impact on test performance characteristics.