scholarly journals Enhanced Eye Velocity in Head Impulse Testing—A Possible Indicator of Endolymphatic Hydrops

2021 ◽  
Vol 8 ◽  
Author(s):  
Ian S. Curthoys ◽  
Leonardo Manzari ◽  
Jorge Rey-Martinez ◽  
Julia Dlugaiczyk ◽  
Ann M. Burgess
Keyword(s):  
Endolymphatic Hydrops ◽  
Physiological Saline ◽  
Prospective Clinical Study ◽  
Systematic Change ◽  
Membranous Labyrinth ◽  
Head Impulse ◽  
Head Velocity ◽  
Head Impulses ◽  
Eye Velocity ◽  
Intake Control

Introduction: On video head impulse testing (vHIT) of semicircular canal function, some patients reliably show enhanced eye velocity and so VOR gains >1.0. Modeling and imaging indicate this could be due to endolymphatic hydrops. Oral glycerol reduces membranous labyrinth volume and reduces cochlear symptoms of hydrops, so we tested whether oral glycerol reduced the enhanced vHIT eye velocity.Study Design: Prospective clinical study and retrospective analysis of patient data.Methods: Patients with enhanced eye velocity during horizontal vHIT were enrolled (n = 9, 17 ears) and given orally 86% glycerol, 1.5 mL/kg of body weight, dissolved 1:1 in physiological saline. Horizontal vHIT testing was performed before glycerol intake (time 0), then at intervals of 1, 2, and 3 h after the oral glycerol intake. Control patients with enhanced eye velocity (n = 4, 6 ears) received water and were tested at the same intervals. To provide an objective index of enhanced eye velocity we used a measure of VOR gain which captures the enhanced eye velocity which is so clear on inspecting the eye velocity records. We call this measure the initial VOR gain and it is defined as: (the ratio of peak eye velocity to the value of head velocity at the time of peak eye velocity). The responses of other patients who showed enhanced eye velocity during routine clinical testing were analyzed to try to identify how the enhancement occurred.Results: We found that oral glycerol caused, on average, a significant reduction in the enhanced eye velocity response, whereas water caused no systematic change. The enhanced eye velocity during the head impulses is due in some patients to a compensatory saccade-like response during the increasing head velocity.Conclusion: The significant reduction in enhanced eye velocity during head impulse testing following oral glycerol is consistent with the hypothesis that the enhanced eye velocity in vHIT may be caused by endolymphatic hydrops.

Role of Muscle Pulleys in Producing Eye Position-Dependence in the Angular Vestibuloocular Reflex: A Model-Based Study

2000 ◽  
Vol 84 (2) ◽  
pp. 639-650 ◽  
Author(s):  
Matthew J. Thurtell ◽  
Mikhail Kunin ◽  
Theodore Raphan
Keyword(s):  
Initial Period ◽  
Semicircular Canals ◽  
Pulse Signal ◽  
Eye Position ◽  
Vestibuloocular Reflex ◽  
Primary Position ◽  
Head Velocity ◽  
Model Based ◽  
Head Impulses ◽  
Eye Velocity

It is well established that the head and eye velocity axes do not always align during compensatory vestibular slow phases. It has been shown that the eye velocity axis systematically tilts away from the head velocity axis in a manner that is dependent on eye-in-head position. The mechanisms responsible for producing these axis tilts are unclear. In this model-based study, we aimed to determine whether muscle pulleys could be involved in bringing about these phenomena. The model presented incorporates semicircular canals, central vestibular pathways, and an ocular motor plant with pulleys. The pulleys were modeled so that they brought about a rotation of the torque axes of the extraocular muscles that was a fraction of the angle of eye deviation from primary position. The degree to which the pulleys rotated the torque axes was altered by means of a pulley coefficient. Model input was head velocity and initial eye position data from passive and active yaw head impulses with fixation at 0°, 20° up and 20° down, obtained from a previous experiment. The optimal pulley coefficient required to fit the data was determined by calculating the mean square error between data and model predictions of torsional eye velocity. For active head impulses, the optimal pulley coefficient varied considerably between subjects. The median optimal pulley coefficient was found to be 0.5, the pulley coefficient required for producing saccades that perfectly obey Listing's law when using a two-dimensional saccadic pulse signal. The model predicted the direction of the axis tilts observed in response to passive head impulses from 50 ms after onset. During passive head impulses, the median optimal pulley coefficient was found to be 0.21, when roll gain was fixed at 0.7. The model did not accurately predict the alignment of the eye and head velocity axes that was observed early in the response to passive head impulses. We found that this alignment could be well predicted if the roll gain of the angular vestibuloocular reflex was modified during the initial period of the response, while pulley coefficient was maintained at 0.5. Hence a roll gain modification allows stabilization of the retinal image without requiring a change in the pulley effect. Our results therefore indicate that the eye position–dependent velocity axis tilts could arise due to the effects of the pulleys and that a roll gain modification in the central vestibular structures may be responsible for countering the pulley effect.

scholarly journals Enhanced Eye Velocity With Backup Saccades in vHIT Tests of a Menière Disease Patient: A Case Report

2021 ◽  
Vol 8 ◽  
Author(s):  
Maria Montserrat Soriano-Reixach ◽  
Jorge Rey-Martinez ◽  
Xabier Altuna ◽  
Ian Curthoys
Keyword(s):  
Disease Patient ◽  
Vestibular Function ◽  
Position Error ◽  
Head Movements ◽  
Slow Phase ◽  
Head Impulse ◽  
Head Impulses ◽  
Eye Velocity ◽  
Gaze Position ◽  
Horizontal Head

Reduced eye velocity and overt or covert compensatory saccades during horizontal head impulse testing are the signs of reduced vestibular function. However, here we report the unusual case of a patient who had enhanced eye velocity during horizontal head impulses followed by a corrective saccade. We term this saccade a “backup saccade” because it acts to compensate for the gaze position error caused by the enhanced velocity (and enhanced VOR gain) and acts to return gaze directly to the fixation target as shown by eye position records. We distinguish backup saccades from overt or covert compensatory saccades or the anticompensatory quick eye movement (ACQEM) of Heuberger et al. (1) ACQEMs are anticompensatory in that they are in the same direction as head velocity and so, act to take gaze off the target and thus require later compensatory (overt) saccades to return gaze to the target. Neither of these responses were found in this patient. The patient here was diagnosed with unilateral definite Meniere's disease (MD) on the right and had enhanced VOR (gain of 1.17) for rightward head impulses followed by backup saccades. For leftwards head impulses eye velocity and VOR gain were in the normal range (VOR gain of 0.89). As further confirmation, testing with 1.84 Hz horizontal sinusoidal head movements in the visual-vestibular (VVOR) paradigm also showed these backup saccades for rightwards head turns but normal slow phase eye velocity responses without backup saccades for leftwards had turns. This evidence shows that backup saccades can be observed in some MD patients who show enhanced eye velocity responses during vHIT and that these backup saccades act to correct for gaze position error caused by the enhanced eye velocity during the head impulse and so have a compensatory effect on gaze stabilization.

Absence of a vergence-mediated vestibulo-ocular reflex gain increase does not preclude adaptation

2021 ◽  
pp. 1-9
Author(s):  
Béla Büki (Family name Büki) ◽  
László T. Tamás (Family name Tamás) ◽  
Christopher J. Todd ◽  
Michael C. Schubert ◽  
Americo A. Migliaccio
Keyword(s):  
Laser Target ◽  
Head Velocity ◽  
Gain Enhancement ◽  
Ocular Reflex ◽  
Vestibulo Ocular Reflex ◽  
Vor Adaptation ◽  
Reflex Gain ◽  
Head Impulses ◽  
Eye Velocity ◽  
Vestibular Pathways

BACKGROUND: The gain (eye-velocity/head-velocity) of the angular vestibuloocular reflex (aVOR) during head impulses can be increased while viewing near-targets and when exposed to unilateral, incremental retinal image velocity error signals. It is not clear however, whether the tonic or phasic vestibular pathways mediate these gain increases. OBJECTIVE: Determine whether a shared pathway is responsible for gain enhancement between vergence and adaptation of aVOR gain in patients with unilateral vestibular hypofunction (UVH). MATERIAL AND METHODS: 20 patients with UVH were examined for change in aVOR gain during a vergence task and after 15-minutes of ipsilesional incremental VOR adaptation (uIVA) using StableEyes (a device that controls a laser target as a function of head velocity) during horizontal passive head impulses.A 5 % aVOR gain increase was defined as the threshold for significant change. RESULTS: 11/20 patients had >5% vergence-mediated gain increase during ipsi-lesional impulses. For uIVA, 10/20 patients had >5% ipsi-lesional gain increase. There was no correlation between the vergence-mediated gain increase and gain increase after uIVA training. CONCLUSION: Vergence-enhanced and uIVA training gain increases are mediated by separate mechanisms and/or vestibular pathways (tonic/phasic).The ability to increase the aVOR gain during vergence is not prognostic for successful adaptation training.

Vertical Eye Position–Dependence of the Human Vestibuloocular Reflex During Passive and Active Yaw Head Rotations

1999 ◽  
Vol 81 (5) ◽  
pp. 2415-2428 ◽  
Author(s):  
Matthew J. Thurtell ◽  
Ross A. Black ◽  
G. Michael Halmagyi ◽  
Ian S. Curthoys ◽  
Swee T. Aw
Keyword(s):  
Three Dimensional ◽  
Head Position ◽  
Eye Position ◽  
Vestibuloocular Reflex ◽  
Head Velocity ◽  
High Acceleration ◽  
Position Dependence ◽  
Head Impulses ◽  
Eye Velocity ◽  
Head Rotations

Vertical eye position–dependence of the human vestibuloocular reflex during passive and active yaw head rotations. The effect of vertical eye-in-head position on the compensatory eye rotation response to passive and active high acceleration yaw head rotations was examined in eight normal human subjects. The stimuli consisted of brief, low amplitude (15–25°), high acceleration (4,000–6,000°/s2) yaw head rotations with respect to the trunk (peak velocity was 150–350°/s). Eye and head rotations were recorded in three-dimensional space using the magnetic search coil technique. The input-output kinematics of the three-dimensional vestibuloocular reflex (VOR) were assessed by finding the difference between the inverted eye velocity vector and the head velocity vector (both referenced to a head-fixed coordinate system) as a time series. During passive head impulses, the head and eye velocity axes aligned well with each other for the first 47 ms after the onset of the stimulus, regardless of vertical eye-in-head position. After the initial 47-ms period, the degree of alignment of the eye and head velocity axes was modulated by vertical eye-in-head position. When fixation was on a target 20° up, the eye and head velocity axes remained well aligned with each other. However, when fixation was on targets at 0 and 20° down, the eye velocity axis tilted forward relative to the head velocity axis. During active head impulses, the axis tilt became apparent within 5 ms of the onset of the stimulus. When fixation was on a target at 0°, the velocity axes remained well aligned with each other. When fixation was on a target 20° up, the eye velocity axis tilted backward, when fixation was on a target 20° down, the eye velocity axis tilted forward. The findings show that the VOR compensates very well for head motion in the early part of the response to unpredictable high acceleration stimuli—the eye position– dependence of the VOR does not become apparent until 47 ms after the onset of the stimulus. In contrast, the response to active high acceleration stimuli shows eye position–dependence from within 5 ms of the onset of the stimulus. A model using a VOR-Listing’s law compromise strategy did not accurately predict the patterns observed in the data, raising questions about how the eye position–dependence of the VOR is generated. We suggest, in view of recent findings, that the phenomenon could arise due to the effects of fibromuscular pulleys on the functional pulling directions of the rectus muscles.

scholarly journals Quantifying a Learning Curve for Video Head Impulse Test: Pitfalls and Pearls

2021 ◽  
Vol 11 ◽  
Author(s):  
Athanasia Korda ◽  
Thomas C. Sauter ◽  
Marco Domenico Caversaccio ◽  
Georgios Mantokoudis
Keyword(s):  
Learning Curve ◽  
Vestibular Function ◽  
Head Impulse Test ◽  
Video Head Impulse Test ◽  
Head Acceleration ◽  
Video Instruction ◽  
Head Impulse ◽  
Head Velocity ◽  
Low Head ◽  
Head Impulses

Objective: The video head impulse test (vHIT) is nowadays a fast and objective method to measure vestibular function. However, its usability is controversial and often considered as a test performed by experts only. We sought to study the learning curve of novices and to document all possible mistakes and pitfalls in the process of learning.Methods: In a prospective cohort observational study, we included 10 novices. We tested their ability to perform correctly horizontal head impulses recorded with vHIT. We assessed vHITs in 10 sessions with 20 impulses per session giving a video instruction after the first session (S1) and individual feedback from an expert for session 2 (S2) up to session 10 (S10). We compared VOR gain, the HIT acceptance rate by the device algorithm, mean head velocity, acceleration, excursion, and overshoot between sessions.Results: A satisfying number of accepted HITs (80%) was reached after an experience of 160 vHITs. Mean head velocity between sessions was always in accepted limits. Head acceleration was too low at the beginning (S1) but improved significantly after the video instruction (p = 0.001). Mean head excursion and overshoot showed a significant improvement after 200 head impulses (p < 0.001 each).Conclusions: We showed that novices can learn to perform head impulses invHIT very fast provided that they receive instructions and feedback from an experienced examiner. Video instructions alone were not sufficient. The most common pitfall was a low head acceleration.

Meniere’s attack – a volume or pressure phenomenon?

2020 ◽  
pp. 1-5
Author(s):  
Idir Djennaoui ◽  
Paul Avan
Keyword(s):  
Causal Relationship ◽  
Clinical Picture ◽  
Endolymphatic Hydrops ◽  
Rapid Recovery ◽  
Ménière’S Disease ◽  
Pressure Measurements ◽  
Inflation Pressure ◽  
Membranous Labyrinth ◽  
Electrophysiological Finding ◽  
Electrophysiological Findings

Meniere’s disease (MD) still raises since its discovery in 1860 pathophysiological and etiopathogenical issues. The main pathophysiological feature that has emerged for decades is an anatomic one, the endolymphatic hydrops (EH), defined by the inflation of the endolymphatic part of the membranous labyrinth. However, the causal relationship between EH and MD has not been proven. Several attempts have been achieved in animals to induce EH. The best known is the blockage of the vestibular duct, which causes a chronic volume inflation of the endolymphatic part. This model is characterized by the discrepancy between electrophysiological findings and scala media inflation. Pressure measurements vary among studies. The endolymphatic infusion model, which attempts to model the acute clinical picture of MD consistently shows pressure equilibration between the endolymphatic and perilymphatic compartments, and rapid recovery of the electrophysiological finding once the injection is stopped.

Implications of rotational kinematics for the oculomotor system in three dimensions

1987 ◽  
Vol 58 (4) ◽  
pp. 832-849 ◽  
Author(s):  
D. Tweed ◽  
T. Vilis
Keyword(s):  
Three Dimensional ◽  
Oculomotor System ◽  
Three Dimensions ◽  
Eye Position ◽  
Head Velocity ◽  
Listing’S Law ◽  
Indirect Path ◽  
Dimensional Models ◽  
Three Dimensional Models ◽  
Eye Velocity

1. This paper develops three-dimensional models for the vestibuloocular reflex (VOR) and the internal feedback loop of the saccadic system. The models differ qualitatively from previous, one-dimensional versions, because the commutative algebra used in previous models does not apply to the three-dimensional rotations of the eye. 2. The hypothesis that eye position signals are generated by an eye velocity integrator in the indirect path of the VOR must be rejected because in three dimensions the integral of angular velocity does not specify angular position. Computer simulations using eye velocity integrators show large, cumulative gaze errors and post-VOR drift. We describe a simple velocity to position transformation that works in three dimensions. 3. In the feedback control of saccades, eye position error is not the vector difference between actual and desired eye positions. Subtractive feedback models must continuously adjust the axis of rotation throughout a saccade, and they generate meandering, dysmetric gaze saccades. We describe a multiplicative feedback system that solves these problems and generates fixed-axis saccades that accord with Listing's law. 4. We show that Listing's law requires that most saccades have their axes out of Listing's plane. A corollary is that if three pools of short-lead burst neurons code the eye velocity command during saccades, the three pools are not yoked, but function independently during visually triggered saccades. 5. In our three-dimensional models, we represent eye position using four-component rotational operators called quaternions. This is not the only algebraic system for describing rotations, but it is the one that best fits the needs of the oculomotor system, and it yields much simpler models than do rotation matrix or other representations. 6. Quaternion models predict that eye position is represented on four channels in the oculomotor system: three for the vector components of eye position and one inversely related to gaze eccentricity and torsion. 7. Many testable predictions made by quaternion models also turn up in models based on other mathematics. These predictions are therefore more fundamental than the specific models that generate them. Among these predictions are 1) to compute eye position in the indirect path of the VOR, eye or head velocity signals are multiplied by eye position feedback and then integrated; consequently 2) eye position signals and eye or head velocity signals converge on vestibular neurons, and their interaction is multiplicative.(ABSTRACT TRUNCATED AT 400 WORDS)

Discharge patterns in nucleus prepositus hypoglossi and adjacent medial vestibular nucleus during horizontal eye movement in behaving macaques

1992 ◽  
Vol 68 (1) ◽  
pp. 319-332 ◽  
Author(s):  
J. L. McFarland ◽  
A. F. Fuchs
Keyword(s):  
Eye Movements ◽  
Eye Movement ◽  
Smooth Pursuit ◽  
Vestibular Nucleus ◽  
Medial Vestibular Nucleus ◽  
Eye Position ◽  
Head Velocity ◽  
Firing Rates ◽  
Prepositus Hypoglossi ◽  
Eye Velocity

1. Monkeys were trained to perform a variety of horizontal eye tracking tasks designed to reveal possible eye movement and vestibular sensitivities of neurons in the medulla. To test eye movement sensitivity, we required stationary monkeys to track a small spot that moved horizontally. To test vestibular sensitivity, we rotated the monkeys about a vertical axis and required them to fixate a target rotating with them to suppress the vestibuloocular reflex (VOR). 2. All of the 100 units described in our study were recorded from regions of the medulla that were prominently labeled after injections of horseradish peroxidase into the abducens nucleus. These regions include the nucleus prepositus hypoglossi (NPH), the medial vestibular nucleus (MVN), and their common border (the “marginal zone”). We report here the activities of three different types of neurons recorded in these regions. 3. Two types responded only during eye movements per se. Their firing rates increased with eye position; 86% had ipsilateral “on” directions. Almost three quarters (73%) of these medullary neurons exhibited a burst-tonic discharge pattern that is qualitatively similar to that of abducens motoneurons. There were, however, quantitative differences in that these medullary burst-position neurons were less sensitive to eye position than were abducens motoneurons and often did not pause completely for saccades in the off direction. The burst of medullary burst position neurons preceded the saccade by an average of 7.6 +/- 1.7 (SD) ms and, on average, lasted the duration of the saccade. The number of spikes in the burst was well correlated with saccade size. The second type of eye movement neuron displayed either no discernible burst or an inconsistent one for on-direction saccades and will be referred to as medullary position neurons. Neither the burst-position nor the position neurons responded when the animals suppressed the VOR; hence, they displayed no vestibular sensitivity. 4. The third type of neuron was sensitive to both eye movement and vestibular stimulation. These neurons increased their firing rates during horizontal head rotation and smooth pursuit eye movements in the same direction; most (76%) preferred ipsilateral head and eye movements. Their firing rates were approximately in phase with eye velocity during sinusoidal smooth pursuit and with head velocity during VOR suppression; on average, their eye velocity sensitivity was 50% greater than their vestibular sensitivity. Sixty percent of these eye/head velocity cells were also sensitive to eye position. 5. The NPH/MVN region contains many neurons that could provide an eye position signal to abducens neurons.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Matching the Oculomotor Drive During Head-Restrained and Head-Unrestrained Gaze Shifts in Monkey

2010 ◽  
Vol 104 (2) ◽  
pp. 811-828 ◽  
Author(s):  
Bernard P. Bechara ◽  
Neeraj J. Gandhi
Keyword(s):  
Mean Squared Error ◽  
Vestibular Nuclei ◽  
Cell Types ◽  
Head Movements ◽  
Abducens Nucleus ◽  
Gaze Shifts ◽  
Gaze Shift ◽  
Head Velocity ◽  
Burst Neurons ◽  
Eye Velocity

High-frequency burst neurons in the pons provide the eye velocity command (equivalently, the primary oculomotor drive) to the abducens nucleus for generation of the horizontal component of both head-restrained (HR) and head-unrestrained (HU) gaze shifts. We sought to characterize how gaze and its eye-in-head component differ when an “identical” oculomotor drive is used to produce HR and HU movements. To address this objective, the activities of pontine burst neurons were recorded during horizontal HR and HU gaze shifts. The burst profile recorded on each HU trial was compared with the burst waveform of every HR trial obtained for the same neuron. The oculomotor drive was assumed to be comparable for the pair yielding the lowest root-mean-squared error. For matched pairs of HR and HU trials, the peak eye-in-head velocity was substantially smaller in the HU condition, and the reduction was usually greater than the peak head velocity of the HU trial. A time-varying attenuation index, defined as the difference in HR and HU eye velocity waveforms divided by head velocity [α = ( Ḣhr − Ėhu)/ Ḣ] was computed. The index was variable at the onset of the gaze shift, but it settled at values several times greater than 1. The index then decreased gradually during the movement and stabilized at 1 around the end of gaze shift. These results imply that substantial attenuation in eye velocity occurs, at least partially, downstream of the burst neurons. We speculate on the potential roles of burst-tonic neurons in the neural integrator and various cell types in the vestibular nuclei in mediating the attenuation in eye velocity in the presence of head movements.

Effect of Transverse Temporal Bone Fracture on the Fluid Compartment of the Inner Ear

1979 ◽  
Vol 88 (6) ◽  
pp. 741-748 ◽  
Author(s):  
Syed S. Rizvi ◽  
Kevin P. Gibbin
Keyword(s):  
Hair Cells ◽  
Endolymphatic Hydrops ◽  
Membranous Labyrinth ◽  
Temporal Bone Fracture ◽  
Complete Obstruction ◽  
Vestibular Hair Cells ◽  
Vestibular Aqueduct ◽  
Fluid Compartment ◽  
Temporal Bones ◽  
Transverse Fractures

Five temporal bones exhibiting transverse fractures were studied with a view to determining whether such fractures could lead to symptomatic endolymphatic hydrops. Four out of the five temporal bones showed the fracture line traversing the vestibular aqueduct. Two of these four showed complete obstruction of the endolymphatic duct. One of these had an intact membranous labyrinth and severe endolymphatic hydrops. The other had ruptures of the membranous labyrinth and no hydrops. Three ears exhibited partial preservation of auditory and vestibular hair cells and neurons. These findings are consistent with the concept that a transverse fracture may produce endolymphatic hydrops by obstructing the vestibular aqueduct while preserving enough audiovestibular epithelium and neurons to present as symptomatic Menière's disease.

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