Posture, Gait, Quality of Life, and Hearing with a Vestibular Implant.

BACKGROUND: Bilateral vestibular hypofunction is associated with chronic disequilibrium, postural instability, and unsteady gait owing to failure of vestibular reflexes that stabilize the eyes, head, and body. A vestibular implant may be effective in alleviating symptoms. METHODS: Persons who had had ototoxic (7 participants) or idiopathic (1 participant) bilateral vestibular hypofunction for 2 to 23 years underwent unilateral implantation of a prosthesis that electrically stimulates the three semicircular canal branches of the vestibular nerve. Clinical outcomes included the score on the Bruininks-Oseretsky Test of Motor Proficiency balance subtest (range, 0 to 36, with higher scores indicating better balance), time to failure on the modified Romberg test (range, 0 to 30 seconds), score on the Dynamic Gait Index (range, 0 to 24, with higher scores indicating better gait performance), time needed to complete the Timed Up and Go test, gait speed, pure-tone auditory detection thresholds, speech discrimination scores, and quality of life. We compared participants' results at baseline (before implantation) with those at 6 months (8 participants) and at 1 year (6 participants) with the device set in its usual treatment mode (varying stimulus pulse rate and amplitude to represent rotational head motion) and in a placebo mode (holding pulse rate and amplitude constant). RESULTS: The median scores at baseline and at 6 months on the Bruininks-Oseretsky test were 17.5 and 21.0, respectively (median within-participant difference, 5.5 points; 95% confidence interval [CI], 0 to 10.0); the median times on the modified Romberg test were 3.6 seconds and 8.3 seconds (difference, 5.1; 95% CI, 1.5 to 27.6); the median scores on the Dynamic Gait Index were 12.5 and 22.5 (difference, 10.5 points; 95% CI, 1.5 to 12.0); the median times on the Timed Up and Go test were 11.0 seconds and 8.7 seconds (difference, 2.3; 95% CI, -1.7 to 5.0); and the median speeds on the gait-speed test were 1.03 m per second and 1.10 m per second (difference, 0.13; 95% CI, -0.25 to 0.30). Placebo-mode testing confirmed that improvements were due to treatment-mode stimulation. Among the 6 participants who were also assessed at 1 year, the median within-participant changes from baseline to 1 year were generally consistent with results at 6 months. Implantation caused ipsilateral hearing loss, with the air-conducted pure-tone average detection threshold at 6 months increasing by 3 to 16 dB in 5 participants and by 74 to 104 dB in 3 participants. Changes in participant-reported disability and quality of life paralleled changes in posture and gait. CONCLUSIONS: Six months and 1 year after unilateral implantation of a vestibular prosthesis for bilateral vestibular hypofunction, measures of posture, gait, and quality of life were generally in the direction of improvement from baseline, but hearing was reduced in the ear with the implant in all but 1 participant. (Funded by the National Institutes of Health and others; ClinicalTrials.gov number, NCT02725463.).

Evidence for the differential efficacy of yaw and pitch gaze stabilization mechanisms in people with multiple sclerosis.

People with multiple sclerosis (PwMS) who report dizziness often have gaze instability due to vestibulo-ocular reflex (VOR) deficiencies and compensatory saccade (CS) abnormalities. Herein, we aimed to describe and compare the gaze stabilization mechanisms for yaw and pitch head movements in PwMS. Thirty-seven PwMS (27 female, mean ± SD age = 53.4 ± 12.4 years old, median [IQR] Expanded Disability Status Scale Score = 3.5, [1.0]. We analyzed video head impulse test results for VOR gain, CS frequency, CS latency, gaze position error (GPE) at impulse end, and GPE at 400 ms after impulse start. Discrepancies were found for median [IQR] VOR gain in yaw (0.92 [0.14]) versus pitch-up (0.71 [0.44], p < 0.001) and pitch-down (0.81 [0.44], p = 0.014]), CS latency in yaw (258.13 [76.8]) ms versus pitch-up (208.78 [65.97]) ms, p = 0.001] and pitch-down (132.17 [97.56] ms, p = 0.006), GPE at impulse end in yaw (1.15 [1.85] degs versus pitch-up (2.71 [3.9] degs, p < 0.001), and GPE at 400 ms in yaw (-0.25 [0.98] degs) versus pitch-up (1.53 [1.07] degs, p < 0.001) and pitch-down (1.12 [1.82] degs, p = 0.001). Compared with yaw (0.91 [0.75]), CS frequency was similar for pitch-up (1.03 [0.93], p = 0.999) but lower for pitch-down (0.65 [0.64], p = 0.023). GPE at 400 ms was similar for yaw and pitch-down (1.88 [2.76] degs, p = 0.400). We postulate that MS may have preferentially damaged the vertical VOR and saccade pathways in this cohort.

Visual vertigo and motion sickness is different between persistent postural-perceptual dizziness and vestibular migraine.

INTRODUCTION: Persistent postural-perceptual dizziness (PPPD) and vestibular migraine (VM) share symptoms of visual vertigo and motion sickness that can be confusing for clinicians to distinguish. We compare the severity of these symptoms and dynamic subjective visual vertical (dSVV) in these two common vestibular conditions. METHOD: Twenty-nine patients with PPPD, 37 with VM, and 29 controls were surveyed for subjective symptoms using the visual vertigo analogue scale (VVAS) and motion sickness susceptibility questionnaire during childhood (MSA) and the past 10 years (MSB). dSVV is a measure of visual dependence measures perception of verticality against a rotating background (5 deg./s). RESULTS: VVAS revealed contextual differences for dizziness between those with PPPD and VM. Ratings of visual vertigo were most severe in PPPD, less in VM, and mild in controls (VVAS PPPD 27.1, VM 11.2, control 4.6, p < 0.001). MSA was more severe in VM than in PPPD or control (12.8 vs 7.6 vs 8.5, p = 0.01). MSB was more severe in VM than controls (MSB score 12.9 VS 8.1 p = 0.009) but was not different than PPPD (MSB score 10.0, p = 0.10). dSVV alignment was similar among the three groups (p = 0.83). Both VM and PPPD groups had greater simulator sickness than controls after completing the dSVV. CONCLUSIONS: Patients with PPPD report more visual vertigo than those with VM, but a history of motion sickness as a child is more common in VM. Additionally, the environmental context that induces visual vertigo is different between PPPD and VM.

Compensatory saccades differ between those with vestibular hypofunction and multiple sclerosis pointing to unique roles for peripheral and central vestibular inputs.

Individuals with peripheral or central vestibular dysfunction recruit compensatory saccades (CSs) in response to high acceleration, yaw head impulses. Although CSs have been shown to be an effective strategy for reducing gaze position error (GPE) in individuals with peripheral hypofunction, for individuals with central vestibular dysfunction, the effectiveness of CS is unknown. The purpose of our study was to compare the effectiveness of CS, defined as the ability to compensate for head velocity and eye position errors, between persons with central and peripheral vestibular dysfunction. We compared oculomotor responses during video head impulse testing between individuals with unilateral peripheral vestibular deafferentation, a disorder of the peripheral vestibular afferents, and individuals with multiple sclerosis, a condition affecting the central vestibular pathways. We hypothesized that relative to individuals with peripheral lesions, individuals with central dysfunction would recruit CSs that were delayed and inappropriately scaled to head velocity and GPE. We show that CSs recruited by persons with central vestibular pathology were not uniformly deficient but instead were of a sufficient velocity to compensate for reductions in VOR gain. Compared to those with peripheral vestibular lesions, individuals with central pathology also recruited earlier covert CS with amplitudes that were better corrected for GPE. Conversely, those with central lesions showed greater variability in the amplitude of overt CS relative to GPE. These data point to a unique role for peripheral and central vestibular inputs in the recruitment of CS and suggest that covert CSs are an effective oculomotor strategy for individuals with multiple sclerosis.NEW & NOTEWORTHY Compensatory saccades (CSs) are recruited by individuals with unilateral vestibular deafferentation (UVD) to compensate for an impaired vestibulo-ocular reflex (VOR). The effectiveness of CS in multiple sclerosis (MS), a central vestibular impairment, is unknown. We show that in UVD and in MS, covert CSs compensate for reduced VOR gain and minimize gaze position error (GPE), yet in >50% of individuals with MS, overt CS worsened GPE, suggesting unique roles for peripheral and central vestibular inputs.

Prevalence of and Theoretical Explanation for Type 2 Benign Paroxysmal Positional Vertigo.

BACKGROUND AND PURPOSE: A variant of benign paroxysmal positional vertigo (BPPV) involves the subjective report of vertigo without the coinciding nystagmus. This presentation includes truncal retropulsion when sitting up from the ipsilesional provocative test (ie, Dix-Hallpike), which we term type 2 BPPV. The primary objective of this study is to prospectively determine the prevalence and describe the clinical course of type 2 BPPV. We offer a theoretical explanation for the absence of nystagmus. METHODS: Prospective, observational study carried out in 2 tertiary hospitals. One hundred eighty patients (134 women, 46 men) met the inclusion criteria and were included between January 10, 2018, and October 30, 2019. Efficacy of physical therapy maneuvers was determined at 1-week follow-up. Three-dimensional reconstructions of the planes of the semicircular canal cupula from histological preparations are offered as evidence for the theoretical explanation. RESULTS: One-third of the patients met the criteria for type 2 BPPV; the remainder had typical posterior or horizontal semicircular canal involvement. Symptoms from type 2 BPPV were longer in duration yet responded favorably to physical therapy maneuvers. Upon repeat testing, 19 patients treated for posterior canalithiasis developed a slight, persistent positional downbeat nystagmus in the Dix-Hallpike position that we propose as evidence the otoconia entered the short arm of the posterior semicircular canal. DISCUSSION AND CONCLUSIONS: Our data and 3-dimensional rendering suggest the report of vertigo, yet absent nystagmus in type 2 BPPV is from otoconia aligning with the gravitoinertial vector during provocative testing that precludes cupular stimulation. Type 2 BPPV appears to be a common and treatable form of vertigo.Video Abstract available for more insights from the authors (see Video, Supplemental Digital Content 1 available at: http://links.lww.com/JNPT/A372).

Head movement kinematics are altered during balance stability exercises in individuals with vestibular schwannoma.

BACKGROUND: Balance stabilization exercises are often prescribed to facilitate compensation in individuals with vestibular schwannoma (VS). However, both the assessment and prescription of these exercises are reliant on clinical observations and expert opinion rather than on quantitative evidence. The aim of this study was to quantify head motion kinematics in individuals with vestibular loss while they performed commonly prescribed balance stability exercises. METHODS: Using inertial measurement units, head movements of individuals with vestibular schwannoma were measured before and after surgical deafferentation and compared with age-matched controls. RESULTS: We found that individuals with vestibular schwannoma experienced more variable head motion compared to healthy controls both pre- and postoperatively, particularly in absence of visual input, but that there was little difference between preoperative and postoperative kinematic measurements for our vestibular schwannoma group. We further found correlations between head motion kinematic measures during balance exercises, performed in the absence of visual input, and multiple clinical measurements for preoperative VS subjects. Subjects with higher head motion variability also had worse DVA scores, moved more slowly during the Timed up and Go and gait speed tests, and had lower scores on the functional gait assessment. In contrast, we did not find strong correlations between clinical measures and postoperative head kinematics for the same VS subjects. CONCLUSIONS: Our data suggest that further development of such metrics based on the quantification of head motion has merit for the assessment and prescription of balance exercises, as demonstrated by the calculation of a "kinematic score" for identifying the most informative balance exercise (i.e., "Standing on foam eyes closed").

An Algorithm for the Diagnosis of Vestibular, Cerebellar, and Oculomotor Disorders Using a Systematized Clinical Bedside Examination.

The bedside examination associated with their clinical history remains the most critical means to accurately diagnose the cause for most of the signs and symptoms related to pathology of the cerebellum and vestibular system in patients presenting with dizziness and imbalance. This paper focuses on those critical bedside examinations, suggests when laboratory testing might be useful to confirm the clinical suspicion, and considers the shared neural circuitry within the visual and vestibular systems to offer an algorithmic approach in conducting the clinical bedside examination.

Vergence increases the amplitude of lateral ocular vestibular evoked myogenic potentials.

The angular and linear vestibulo-ocular reflex responses are greater when viewing near targets to compensate for the relatively larger translation of the eyes with respect to the target. Our aim was to measure vestibular evoked myogenic potentials using a lateral ocular electrode montage (oVEMP) with a laterally applied stimulus using a mini-shaker during both far- and near-viewing (vergence) distances to determine whether vergence affects the oVEMP response as it does the semicircular canal vestibulo-ocular reflex response. Our results show that during vergence, the p1 and n1-p1 amplitude of the lateral oVEMP response increases significantly, whereas the latencies do not change significantly. We suggest that the physiological basis for this vergence-mediated amplitude increase in potentials may be the same as those already documented using transient linear head accelerations. Our data also suggest that irregular vestibular afferents are likely mediating the vergence-mediated gain increase during linear head accelerations because only irregular afferents are stimulated during short, transient 500 Hz stimuli.

Convergence Vestibulo-ocular Reflex in Unilateral Vestibular Hypofunction: Behavioral Evidence in Support of a Novel Gaze Stability Exercise.

BACKGROUND AND PURPOSE: Convergence of the eyes during head rotation increases the gain (eye velocity/head velocity) of the vestibulo-ocular reflex (VOR). We sought to know whether convergence would increase the VOR gain (mean + SD) in unilateral vestibular hypofunction (UVH). METHODS: Vestibulo-ocular reflex gain during ipsi- and contralesional horizontal head rotation at near (15 cm) and far (150 cm) targets was measured in 22 subjects with UVH and 12 healthy controls. Retinal slip was estimated (retinal slip index [RSI]) as the difference between ideal VOR gain (no retinal slip) and the actual VOR gain. RESULTS: Convergence did not significantly enhance VOR gain for ipsilesional rotation (mean difference, 0.04; 95% confidence interval [CI], -0.01 to 0.09), near viewing (0.77 ± 0.34) versus far viewing (0.72 ± 0.29), yet the VOR gain during contralesional rotation was greater for near viewing (1.20 ± 0.23) than for far viewing (0.97 ± 0.21; mean difference, 0.23; 95% CI, 0.13-0.32). In the 36% of subjects with recovery of their ipsilesional VOR gain, the vergence effect trended to recover (far VOR gain: 1.06 ± 0.17 vs near VOR gain 1.16 ± 0.21; mean difference, 0.10; 95% CI, -0.02 to 0.22). Ipsilesional head rotation induced greater retinal slip for near (RSI = 0.90 ± 0.34) targets than for far targets (RSI = 0.35 ± 0.29; mean difference, 0.56; 95% CI, 0.51-0.61). DISCUSSION AND CONCLUSIONS: The convergence-mediated VOR gain enhancement is preserved during contralesional but impaired during ipsilesional head rotation. Recovery of ipsilesional passive VOR gain does not equate to restored convergence enhancement, although it did increase ∼10%. These data suggest head motion viewing near targets will increase retinal slip, which warrants consideration as a gaze stability exercise for subjects with UVH.Video Abstract available for more insights from the authors (see Video, Supplemental Digital Content 1, available at: http://links.lww.com/JNPT/A325).

Comparison of Incremental Vestibulo-ocular Reflex Adaptation Training Versus x1 Training in Patients With Chronic Peripheral Vestibular Hypofunction: A Two-Year Randomized Controlled Trial.

BACKGROUND AND PURPOSE: A crossover, double-blinded randomized controlled trial to investigate once-daily incremental vestibulo-ocular reflex (VOR) adaptation (IVA) training over 2 years in people with stable and chronic peripheral vestibular hypofunction. METHODS: Twenty-one patients with peripheral vestibular hypofunction were randomly assigned to intervention-then-control (n = 12) or control-then-intervention (n = 9) groups. The task consisted of either x1 (control) or IVA training, once daily every day for 15 minutes over 6-months, followed by a 6-month washout, then repeated for arm 2 of the crossover. Primary outcome: vestibulo-ocular reflex gain. Secondary outcomes: compensatory saccades, dynamic visual acuity, static balance, gait, and subjective symptoms. Multiple imputation was used for missing data. Between-group differences were analyzed using a linear mixed model with repeated measures. RESULTS: On average patients trained once daily 4 days per week. IVA training resulted in significantly larger VOR gain increase (active: 20.6% ± 12.08%, P = 0.006; passive: 30.6% ± 25.45%, P = 0.016) compared with x1 training (active: -2.4% ± 12.88%, P = 0.99; passive: -0.6% ± 15.31%, P = 0.68) (P < 0.001). The increased IVA gain did not significantly reduce with approximately 27% persisting over the washout period. x1 training resulted in greater reduction of compensatory saccade latency (P = 0.04) and increase in amplitude (P = 0.02) compared with IVA training. There was no difference between groups in gait and balance measures; however, only the IVA group had improved total Dizziness Handicap Inventory (P = 0.006). DISCUSSION AND CONCLUSIONS: Our results suggest IVA improves VOR gain and reduces perception of disability more than conventional x1 training. We suggest at least 4 weeks of once-daily 4 days-per-week IVA training should be part of a comprehensive vestibular rehabilitation program.Video Abstract available for more insights from the authors (see the Video, Supplemental Digital Content 1, available at: http://links.lww.com/JNPT/A356).

Once-Daily Incremental Vestibular-Ocular Reflex Adaptation Training in Patients With Chronic Peripheral Vestibular Hypofunction: A 1-Week Randomized Controlled Study.

BACKGROUND AND PURPOSE: This was a double-blinded randomized controlled study to investigate the effects of once-daily incremental vestibulo-ocular reflex (VOR) training over 1 week in people with chronic peripheral vestibular hypofunction. METHODS: A total of 24 patients with peripheral vestibular hypofunction were randomly assigned to intervention (n = 13) or control (n = 11) groups. Training consisted of either x1 (control) or incremental VOR adaptation exercises, delivered once daily for 15 minutes over 4 days in 1 week. Primary outcome: VOR gain with video-oculography. Secondary outcomes: Compensatory saccades measured using scleral search coils, dynamic visual acuity, static balance, gait, and subjective symptoms. Between-group differences were analyzed with a linear mixed-model with repeated measures. RESULTS: There was a difference in the VOR gain increase between groups (P < 0.05). The incremental training group gain increased during active (13.4% ± 16.3%) and passive (12.1% ± 19.9%) head impulse testing (P < 0.02), whereas it did not for the control group (P = 0.59). The control group had reduced compensatory saccade latency (P < 0.02). Both groups had similarly improved dynamic visual acuity scores (P < 0.05). Both groups had improved dynamic gait index scores (P < 0.002); however, only the incremental group had improved scores for the 2 walks involving head oscillations at approximately 2 Hz (horizontal: P < 0.05; vertical: P < 0.02), increased gait speed (P < 0.02), and step length (P < 0.01) during normal gait, and improved total Dizziness Handicap Inventory (P < 0.05). CONCLUSIONS: Our results suggest incremental VOR adaptation significantly improves gain, gait with head rotation, balance during gait, and symptoms in patients with chronic peripheral vestibular hypofunction more so than conventional x1 gaze-stabilizing exercises.Video Abstract available for more insights from the authors (see the Video, Supplemental Digital Content 1, available at: http://links.lww.com/JNPT/A336).

Evidence a shared mechanism mediates ipsi- and contralesional compensatory saccades and gait after unilateral vestibular deafferentation.

The study objective was to understand how the contralesional labyrinth contributes to gaze and gait stability after unilateral vestibular deafferentation (UVD). Head impulse testing (vHIT) was completed in 37 individuals [22 women (59%); age 52.13 ± 11.59 yr, mean ± SD] with UVD from vestibular schwannoma resection. Compensatory saccades (CS) and vestibulo-ocular reflex (VOR) gain were analyzed for both ipsilesional and contralesional impulses. Gait speed (10-m walk test) and endurance (2-min walk test) were collected for 35 individuals. CS were recruited during contralesional head rotation regardless of VOR gain on either the ipsilesional [ρ = 0.21 (-0.14, 0.57); Spearman rank (95% confidence interval)] or contralesional side [ρ = -0.04 (-0.42, 0.35)]. Additionally, the latency of these CS (151.19 ± 52.41 ms) was similar to that of CS generated during ipsilesional rotation (165.65 ± 21.62 ms; P = 0.159). CS recruited during ipsilesional vHIT were of a higher velocity (P < 0.001) and greater frequency (P < 0.001) compared with contralesional CS. VOR gain asymmetry was significantly correlated with gait speed [ρ = -0.37 (-0.73, -0.01)], yet individual VOR gain was not correlated [ipsilesional: ρ = 0.17 (-0.20, 0.55); contralesional: ρ = -0.18 (-0.52, 0.15)]. Our data reveal CS are recruited at similar latencies without correlation to VOR gain or direction of head rotation, and that the central integration of ipsilesional and contralesional vestibular afference correlates with gait. Together, our data suggest the brain considers vestibular afference from both sides when generating related behavioral output after UVD.NEW & NOTEWORTHY After unilateral vestibular deafferentation, compensatory saccades (CS) have similar latencies regardless of the direction of head rotation, and those CS generated during contralesional head rotation are unrelated to extent of vestibular loss. Additionally, the extent of asymmetry in residual vestibular function, not the extent of vestibular loss, correlates with gait speed. Our data suggest a common mechanism is responsible for the generation of CS and restoration of gait speed in vestibular compensation.

The instantaneous training demand drives vestibulo-ocular reflex adaptation.

The vestibulo-ocular reflex (VOR) maintains stable vision during rapid head rotations by rotating the eyes in the opposite direction to the head. The latency between onset of the head rotation and onset of the eye rotation is 5-8 ms in healthy humans. However, VOR latency can be 3-4 times larger in patients treated with intra-tympanic gentamicin. A prior study showed that latency can be trained with head rotations at 0.2 Hz. We sought to determine how the VOR is affected when a delay between vestibular and visual stimuli is added during adaptation training with high-frequency head rotations (impulses), where the VOR is the main vision-stabilizing system. Using a variant of the incremental VOR adaptation technique, the delay between head rotation onset and movement onset of a visual target was gradually increased. With this training, the instantaneous VOR gain demand (= target/head velocity) varied from less than unity to greater than unity during each head impulse, albeit in a consistent and repeatable way. We measured the active and passive VOR gain and latency before and after VOR adaptation training in healthy normal subjects. There was no significant change in VOR latency across subjects; however, there was a significant decrease in VOR gain of - 6.0 ± 4.5%. These data suggest that during high-frequency head rotations delay/latency is interpreted as a changing instantaneous VOR gain demand. Although the gain demand in this study had a complex trajectory, adaptation was evident with the VOR seeming to use an average of the instantaneous gain demand.

New advances regarding adaptation of the vestibulo-ocular reflex.

This is a review summarizing the development of vestibulo-ocular reflex (VOR) adaptation behavior with relevance to rehabilitation over the last 10 years and examines VOR adaptation using head-on-body rotations, specifically the influence of training target contrast, position and velocity error signal, active vs. passive head rotations, and sinusoidal vs. head impulse rotations. This review discusses optimization of the single VOR adaptation training session, consolidation between repeated training sessions, and dynamic incremental VOR adaptation. Also considered are the effects of aging and the roles of the efferent vestibular system, cerebellum, and otoliths on angular VOR adaptation. Finally, this review examines VOR adaptation findings in studies using whole body rotations.

Human vestibulo-ocular reflex adaptation is frequency selective.

The vestibulo-ocular reflex (VOR) is the only system that maintains stable vision during rapid head rotations. The VOR gain (eye/head velocity) can be trained to increase using a vestibular-visual mismatch stimulus. We sought to determine whether low-frequency (sinusoidal) head rotation during training leads to changes in the VOR during high-frequency head rotation testing, where the VOR is more physiologically relevant. We tested eight normal subjects over three sessions. For training protocol 1, subjects performed active sinusoidal head rotations at 1.3 Hz while tracking a laser target, whose velocity incrementally increased relative to head velocity so that the VOR gain required to stabilize the target went from 1.1 to 2 over 15 min. Protocol 2 was the same as protocol 1, except that head rotations were at 0.5 Hz. For protocol 3, head rotation frequency incrementally increased from 0.5 to 2 Hz over 15 min, while the VOR gain required to stabilize the target was kept at 2. We measured the active and passive, sinusoidal (1.3Hz) and head impulse VOR gains before and after each protocol. Sinusoidal and head impulse VOR gains increased in protocols 1 and 3; however, although the sinusoidal VOR gain increase was ~20%, the related head impulse gain increase was only ~10%. Protocol 2 resulted in no-gain adaptation. These data show human VOR adaptation is frequency selective, suggesting that if one seeks to increase the higher-frequency VOR response, i.e., where it is physiologically most relevant, then higher-frequency head movements are required during training, e.g., head impulses.NEW & NOTEWORTHY This study shows that human vestibulo-ocular reflex adaptation is frequency selective at frequencies >0.3 Hz. The VOR in response to mid- (1.3 Hz) and high-frequency (impulse) head rotations were measured before and after mid-frequency sinusoidal VOR adaptation training, revealing that the mid-frequency gain change was higher than high-frequency gain change. Thus, if one seeks to increase the higher-frequency VOR response, where it is physiologically most relevant, then higher-frequency head movements are required during training.

The bucket test differentiates patients with MRI confirmed brainstem/cerebellar lesions from patients having migraine and dizziness alone.

BACKGROUND: Amongst the most challenging diagnostic dilemmas managing patients with vestibular symptoms (i.e. vertigo, nausea, imbalance) is differentiating dangerous central vestibular disorders from benign causes. Migraine has long been recognized as one of the most common causes of vestibular symptoms, but the clinical hallmarks of vestibular migraine are notoriously inconsistent and thus the diagnosis is difficult to confirm. Here we conducted a prospective study investigating the sensitivity and specificity of combining standard vestibular and neurological examinations to determine how well central vestibular disorders (CVD) were distinguishable from vestibular migraine (VM). METHOD: Twenty-seven symptomatic patients diagnosed with CVD and 36 symptomatic patients with VM underwent brain imaging and clinical assessments including; 1) SVV bucket test, 2) ABCD2, 3) headache/vertigo history, 4) presence of focal neurological signs, 5) nystagmus, and 6) clinical head impulse testing. RESULTS: Mean absolute SVV deviations measured by bucket testing in CVD and VM were 4.8 ± 4.1° and 0.7 ± 1.0°, respectively. The abnormal rate of SVV deviations (> 2.3°) in CVD was significantly higher than VM (p < 0.001). Using the bucket test alone to differentiate CVD from VM, sensitivity was 74.1%, specificity 91.7%, positive likelihood ratio (LR+) 8.9, and negative likelihood ratio (LR-) 0.3. However, when we combined the SVV results with the clinical exam assessing gaze stability (nystagmus) with an abnormal focal neurological exam, the sensitivity (92.6%) and specificity (88.9%) were optimized (LR+ (8.3), LR- (0.08)). CONCLUSION: The SVV bucket test is a useful clinical test to distinguish CVD from VM, particularly when interpreted along with the results of a focal neurological exam and clinical exam for nystagmus.

Rehabilitation to improve gaze and postural stability in people with multiple sclerosis: study protocol for a prospective randomized clinical trial.

BACKGROUND: The use of vestibular rehabilitation principles in the management of gaze and postural stability impairments in people with multiple sclerosis (PwMS) has shown promise in pilot work completed in our lab and in a recently published randomized clinical trial (RCT). However, further work is needed to fully quantify the gaze and postural impairments present in people with multiple sclerosis and how they respond to rehabilitation. METHODS/DESIGN: The study is a single blind RCT designed to examine the benefit of a gaze and postural stability (GPS) intervention program compared to a standard of care (SOC) rehabilitation program in dizzy and balance impaired PwMS. Outcomes will be collected across the domains of body structure and function, activity, and participation as classified by the World Health Organization International Classification of Functioning, Disability, and Health (ICF). Our primary outcomes are the Dizziness Handicap Inventory (DHI) and the Functional Gait Assessment (FGA). Secondary outcomes include other measures of gaze and postural stability, fatigue, and functional mobility. Participants who are interested and eligible for enrollment will be consented prior to completing a baseline assessment. Following the baseline assessment each participant will be randomized to either the GPS or SOC intervention group and will complete a 6 week treatment period. During the treatment period, both groups will participate in guided exercise 3x/week. Following the treatment period participants will be asked to return for a post-treatment evaluation and again for a follow-up assessment 1 month later. We anticipate enrolling 50 participants. DISCUSSION: This study will be an innovative RCT that will utilize gaze and postural stability metrics to assess the efficacy of vestibular rehabilitation in PwMS. It will build on previous work by examining measures across the ICF and improve the current evidence base for treating PwMS. TRIAL REGISTRATION: ClinicalTrials.gov, May 29th 2018, NCT03521557 .

Ocular Misalignment in Dizzy Patients-Something's A-Skew.

BACKGROUND AND PURPOSE: Both central (eg, brain stem, cerebellum) and peripheral (eg, vestibular, fourth cranial nerve palsy) etiologies can cause a vertical misalignment between the eyes with a resultant vertical diplopia. A vertical binocular misalignment may be due to a skew deviation, which is a nonparalytic vertical ocular misalignment due to roll plane imbalance in the graviceptive pathways. A skew deviation may be 1 component of the ocular tilt reaction. The purposes of this article are (1) to understand the pathophysiology of a skew deviation/ocular tilt reaction and (2) to be familiar with the examination techniques used to diagnose a skew and to differentiate it from mimics such as a fourth cranial nerve palsy. SUMMARY OF KEY POINTS: The presence of a skew deviation usually indicates a brain stem or cerebellar localization. Vertical ocular misalignment is easily missed when observing the resting eye position alone. RECOMMENDATIONS FOR CLINICAL PRACTICE: Physical therapists treating patients with vestibular pathology from central or peripheral causes should screen for vertical binocular disorders.

Incremental Vestibulo-ocular Reflex Adaptation Training Dynamically Tailored for Each Individual.

BACKGROUND AND PURPOSE: Unilateral incremental vestibulo-ocular reflex (VOR) adaptation (IVA) increases the VOR gain (= eye/head velocity) for head rotations to one side by ∼10%. Prior IVA studies involved setting the initial VOR training gain demand at the subject's starting value (= 1 in a healthy subject), with the gain preset to increment by 0.1 every 90 seconds over 15 minutes, defined as Static IVA. We determined whether a dynamically calculated gain demand (= "actual gain" + 0.1) would result in greater adaptation, defined as Dynamic IVA. METHODS: Using a hybrid video-oculography and StableEyes training system, we measured the active (self-generated head impulse) and passive (imposed, unpredictable head impulse) VOR gain in 8 healthy subjects before and after 15 minutes of Static (ie, preset) and Dynamic IVA training consisting of active, leftward and rightward, horizontal head impulses (peak amplitude 15°, peak velocity 150°/s, and peak acceleration 3000°/s). We also measured the active VOR gain during training. RESULTS: The VOR gain increase toward the adapting side was ∼5% larger after Dynamic compared with Static IVA training (Dynamic: 13.9% ± 5.2%, Static: 9.4% ± 7.3%; P < 0.05). DISCUSSION AND CONCLUSIONS: Our data suggest that 17°/s retinal image slip (due to the 0.1 gain difference between demand and actual gain) is sufficient to drive robust VOR adaptation. The implications for vestibular rehabilitation are that Dynamic IVA training not only produces better VOR adaptation but also allows more flexible training, for example, training can be spread over several smaller time blocks, without undoing prior adaptation.

Using Inertial Sensors to Quantify Postural Sway and Gait Performance during the Tandem Walking Test.

Vestibular dysfunction typically manifests as postural instability and gait irregularities, in part due to inaccuracies in processing spatial afference. In this study, we have instrumented the tandem walking test with multiple inertial sensors to easily and precisely investigate novel variables that can distinguish abnormal postural and gait control in patients with unilateral vestibular hypofunction. Ten healthy adults and five patients with unilateral vestibular hypofunction were assessed with the tandem walking test during eyes open and eyes closed conditions. Each subject donned five inertial sensors on the upper body (head, trunk, and pelvis) and lower body (each lateral malleolus). Our results indicate that measuring the degree of balance and gait regularity using five body-worn inertial sensors during the tandem walking test provides a novel quantification of movement that identifies abnormalities in patients with vestibular impairment.