A Novel B-vHIT Classification Framework Enhances Discrimination of Non-Peripheral vs. Peripheral Vertigo

Abstract

Background:: This study aimed to investigate the potential role of binocular video head impulse test (B-vHIT) in distinguishing non-peripheral and peripheral vertigo.

Methods:: A cohort of 46 healthy volunteers underwent B-vHIT to establish normative reference values. Concurrently, 104 patients presenting with acute vertigo (onset ≤ 72 hours) underwent B-vHIT and HINTS protocol. B-vHIT parameters were analyzed according to imaging-supported clinical diagnoses and compared with HINTS results. Further, a four-category framework was proposed to differentiate non-peripheral from peripheral vertigo.

Results:: Significant differences in Interocular Gain Asymmetry (χ² = 68.381, P < 0.001) and Interocular Gain Difference (χ² = 50.187, P < 0.001) were observed among groups, revealing a post-hoc hierarchical pattern in which peripheral ophthalmoplegic-related dizziness (POD) group had the highest values, followed by central vertigo, peripheral vertigo and healthy controls. An Asymmetry threshold of < 16 combined with a Difference threshold of < 0.2 achieved 86.4% sensitivity and 89.2% specificity in distinguishing non-peripheral from peripheral causes of vertigo. The Type I (Gain−, Difference−) and Type IV (Gain+, Difference+) patterns demonstrated high specificity (99%) and sensitivity (79%) for identifying non-peripheral vertigo.

Conclusion:: The B-vHIT can serve as a useful tool to distinguish between two types vertigo. The classification framework integrating Gain and Difference should be further investigated for distinguishing non-peripheral vertigo from peripheral vertigo.

Keywords

central vertigo / HINTS / peripheral vestibular disorders / binocular-vHIT

1 Introduction

Dizziness is the third most common major medical symptom reported in general medical clinics, affecting approximately 20%–40% of the general population^[1]. Previous studies have shown that the incidence rates of dizziness increase with age, rising to 39% in individuals over 80 years of age^[2]. It is crucial to differentiate peripheral causes of vertigo, such as vestibular neuritis, from more serious central causes, such as strokes affecting the cerebellum or brainstem^[3]. The head impulse test (HIT) is commonly used as a bedside examination for patients with acute vertigo, helping to distinguish peripheral vertigo from central vertigo. It evaluates the vestibulo-ocular reflex (VOR) pathway by quickly and unpredictably rotating the head, by stimulating the ampullae within the horizontal semicircular canals to observe whether the eyes remain steadily fixed on the target. To stabilize the image of the visual target on the retina during head movements, a three-neuron reflex arc generates compensatory eye movements opposite to the direction of head acceleration: vestibular afferents project to the vestibular nuclei and then to the oculomotor nuclei^[4]. The video head impulse test (vHIT) provides a more objective method for measuring the eye movement findings of the Head Impulse. Equipped with high-speed camera and gyroscopes, vHIT can accurately record the eye and head movements. By comparing eye and head movement displacements or velocities, it objectively quantifies the VOR gain value and reduces subjective errors.

Traditional vHIT devices typically adopt monocular recording and utilizes monocular gain as the VOR response^[5]. Emerging evidence highlights limitations of monocular vHIT when used in isolation. Specifically, monocular vHIT may yield false-positive results that resemble peripheral vestibular dysfunction when non-peripheral lesions disrupt the VOR pathways through direct neural pathway injury or secondary to oculomotor lesion ^[6-^8]. Prior studies have demonstrated that a subset of patients with central vestibular disorders, particularly those involving combined peripheral and central pathologies or circumscribed brainstem/cerebellar lesions, may exhibit reduced VOR gain on HIT/vHIT^[9-^12]. For instance, patients with acute unilateral vestibular nuclei infarction or cerebellar strokes can present with ipsilateral horizontal-canal vHIT gain reductions comparable to peripheral vestibulopathy, potentially leading to diagnostic ambiguity^[13, ^14]. In addition, a subset of patients with central vestibulopathy may exhibit binocular non-conjugation, resulting in inconsistent VOR response of two eyes^[15].

The advent of binocular video head impulse testing (B-vHIT) offers novel prospects for VOR assessment, potentially reducing misdiagnosis of non-peripheral vertigo. In this study, we recruited healthy participants to establish normative reference values for B-vHIT. Furthermore, we assessed patients with acute peripheral and non-peripheral vestibular vertigo using B-vHIT, with the goal of identifying new parameters that can effectively distinguish non-peripheral vertigo from peripheral vertigo.

2 Materials and Methods

This study was conducted at the Vertigo Clinic at Eye and ENT Hospital of Fudan University. The study strictly followed the ethical standards in the Declaration of Helsinki and was approved by the Institutional Review Board (No.2023178, ChiCTR2400089341). All participants provided written informed consent.

2.1 Participants

This study was conducted between December 2023 and September 2024. During the study period, 680 patients presenting with acute vertigo or dizziness came to the Vertigo clinic. The inclusion criteria were a chief complaint of persistent vertigo or dizziness, with or without nausea, vomiting, unsteady gait or balance disorders or spontaneous nystagmus. Patients younger than 18 years old and those who presented more than 72 hours after symptom onset were excluded. In addition, episodic vertigo with a definitive diagnosis, such as benign paroxysmal positional vertigo (BPPV), vestibular migraine (VM), or Ménière’s disease (MD) was excluded.

Additionally, we included a control group comprising 46 healthy subjects aged 20 to 40 years. These individuals had no history of vestibular problems, otological, or neurological disorders, and exhibited no abnormalities in posture, gait, eye diseases, or severe cervical spondylosis. The enrollment flowchart is shown in Figure 1.

2.2 Diagnostic classification

All enrolled patients underwent a comprehensive assessment conducted by vertigo specialists to establish their diagnoses. If neuroimaging findings or clinical signs suggested central involvement, patients were referred to neurologists for further evaluation. Specifically, neurologists made a diagnosis of central vertigo and peripheral ophthalmoplegic-related dizziness (POD), while vertigo specialists made a diagnosis of peripheral vertigo. In cases of diagnostic disagreement, a senior neurologist and a vertigo specialist jointly made the final diagnosis based on imaging and clinical follow-up.

This diagnostic process incorporated three key components: 1) standardized neurological physical examination, 2) quantitative ocular motor assessments, including videonystagmography, and 3) confirmatory neuroimaging studies. All enrolled patients with vertigo underwent computed tomography (CT) scan or brain magnetic resonance imaging (MRI).

Central vertigo can be precisely localized to the site of neurological lesions using MRI or CT^[16]. Peripheral vestibular lesions were diagnosed when central ocular motor signs were absent and imaging findings, examination and clinical follow-up were normal. POD refers to dizziness resulting from uncoordinated eye movements caused by damage to the extraocular muscles or the cranial nerves that control them (oculomotor nerve CN III, trochlear nerve CN IV and abducens nerve CN VI), leading to a mismatch with the visual information transmitted to the brain and disrupting the brain’s normal perception of space and motion. The specific definition and range of lesions is illustrated in Figure 2.

3 Protocol and Parameters

The binocular-vHIT was performed using the VertiGoggles® ZT-VNG-II, manufactured by Shanghai ZEHNI Medical Technology Co., Ltd., Shanghai, China. Unlike monocular vHIT systems, two infrared video cameras are mounted on the left and right sides of the goggles, enabling simultaneous acquisition of left- and right-eye movements for synchronized digital recording, real-time monitoring, and analysis. The goggles are secured tightly to the head with an adjustable elastic strap to avoid slippage during impulses. Testing was conducted in a well-lit room to ensure clear imaging of pupil. Calibration involved participants keeping their head still and viewing a randomly jumping target placed 1.2m ahead. After calibration, participants were instructed to gaze on the target while the examiner performed abrupt, unpredictable head impulses. Each pair of semicircular canals (SCCs) was tested, including the right-left lateral, left posterior-right anterior, and right posterior-left anterior. For vertical canal testing, participants were rotated 30–40 degrees to the left or right away from the mid-sagittal plane. The examiner delivered fast, low-amplitude (10°–20°) head rotations in a randomized order, with at least 15 impulses per SCC pair. All B-vHIT examinations were performed by an experienced technician.

To quantify the difference in gain between two eyes, we proposed two novel indicators for B-vHIT, namely Interocular Gain Asymmetry and Interocular Gain Difference, based on the binocular vHIT. Firstly, we tested whether Asymmetry and Difference could assist in differentiating non-peripheral vertigo from peripheral vertigo. According to the results, we established a four-tier diagnostic categorization: type I Gain (−) Difference (−); type II Gain (−) Difference (+); type III Gain (+) Difference (−); type IV Gain (+) Difference (+). Gain (+) was defined as a gain value of < 0.7 for vertical SCCs or < 0.8 for horizontal SCCs in either eye. Asymmetry and Difference were calculated by using the following formulae:

\mathit{A}\mathit{s}\mathit{y}\mathit{m}\mathit{m}\mathit{e}\mathit{t}\mathit{r}\mathit{y}=\left(\frac{\mathit{R}-\mathit{L}}{\mathit{R}+\mathit{L}}\right)\mathbf{\ast }\mathbf{100}

\mathit{D}\mathit{i}\mathit{f}\mathit{f}\mathit{e}\mathit{r}\mathit{e}\mathit{n}\mathit{c}\mathit{e}=|\mathit{R}-\mathit{L}|

R indicated the gain of the right eye; L indicated the gain of the left eye.

3.1 Comparison of B-vHIT with HINTS Protocol

The Head-Impulse-Nystagmus-Test of Skew (HINTS) protocol is recognized as the clinical gold standard for distinguishing central vertigo from peripheral vertigo. To evaluate the incremental value of B-vHIT and potential synergistic effect, all 104 enrolled patients underwent both B-vHIT and HINTS, and the diagnostic performance was compared.

3.2 Statistical analysis

Statistical analyses were performed using IBM SPSS Statistics Version 29 for macOS. The Shapiro-Wilk test was used to assess the normal distribution of each variable by calculating the W statistic. Variables were expressed as the interquartile ranges (IQRs) when the data didn’t follow a normal distribution. Non-parametric tests and independent- sample median test were used to compare differences between 2 or more groups, and post hoc comparisons using the Bonferroni method. The receiver operating characteristic (ROC) analysis and Youden’s index were conducted for VOR Gain Asymmetry and Difference to ascertain sensitivity and specificity, as well as to identify the optimal threshold values. For inter-rater reliability, Cohen’s kappa was calculated to assess the agreement between raters for B-vHIT results and imaging-based clinical diagnoses. Differences were considered statistically significant when the P < 0.05.

4 Results

The study cohort included 46 healthy controls (28 females [60.9%], 18 males [39.1%]) with a mean age of 34.82 ± 10.34 years (range, 20–40 years). Normative B-vHIT parameters established for this control group are detailed in Table 1.

We screened 248 patients with acute vertigo and excluded 144 patients for a history of recurrent vertigo or dizziness (68 with BPPV, 39 with MD, and 37 with VM). Among the 104 patients enrolled in this study, peripheral vestibular vertigo accounted for 68% (71/104), central vertigo for 23% (24/104), and POD for 8% (9/104) according to the classification of the etiology of the patients. An overview of patient demographics and clinical characteristics is presented in Table 2.

By comparing Asymmetry and Difference in abnormal SCCs, we found significant differences among the healthy, peripheral vertigo, central vertigo, and POD groups (χ²₁ = 68.381, P₁ < 0.001; χ²₂ = 50.187, P₂ < 0.001, respectively). The results of post-hoc comparisons indicated that, based on Asymmetry and Difference values, the ranking from highest to lowest was as follows: POD, central vertigo, peripheral vertigo, and healthy individuals. Unlike Asymmetry, there was no significant difference in the parameter Difference between the healthy group and the peripheral vertigo group (Figure 3).

The ROC curve indicated that an Asymmetry of < 16 demonstrated 86.4% (95% confidence interval [CI]: 72.0% to 94.3%) specificity and 88.2% (95% CI: 80.0% to 93.5%) sensitivity for distinguishing peripheral vertigo from non-peripheral vertigo (central vertigo and POD). The ROC curve analysis further confirmed the diagnostic utility of the Interocular Gain Difference derived from B-vHIT, showing a specificity and sensitivity of 86.4% (95% CI: 72.0% to 94.3%) and 98% (95% CI: 92.4% to 99.7%), respectively, for this differentiation. The optimal cut-off value for this parameter was identified as 0.20. Additionally, considering the distinct impacts of POD and central vertigo on VOR pathways, the Interocular Gain Difference was further analyzed. Specifically, an Interocular Gain Asymmetry > 38 showed a sensitivity of 61.9% (95% CI: 38.7% to 81.0%) and a specificity of 91.3% (95% CI: 70.5% to 98.5%) for distinguishing POD from central vertigo, while the ROC curve revealed that the Interocular Gain Difference in B-vHIT achieved a sensitivity of 76.2% (95% CI: 52.5% to 90.9%) and a specificity of 82.6% (95% CI: 60.4% to 94.3%). The optimal cut-off value for this distinction was determined to be 0.37(Figure 4).

In view of the significant difference in Asymmetry in gain between the healthy group and the peripheral vertigo group, the results of Gain and Difference were categorized to distinguish between peripheral vertigo and non-peripheral vertigo. The classifications were as follows: Type I Gain (−) Difference (−); Type II Gain (−) Difference (+); Type III Gain (+) Difference (−); Type IV Gain (+) Difference (+) (Table 3).

Table 3 presents the distribution of different types of patients. There was good consistency between peripheral vertigo and Type III (κ₁ = 0.91, P₁ < 0.001). Type III demonstrated a sensitivity of 98.5% (95%CI: 91.3% to 99.9%) and a specificity of 90.9% (95%CI: 74.5% to 97.6%) in identifying peripheral diseases. Excellent agreement was also observed between non-peripheral and Types I&IV (κ₂ = 0.813, P₂ < 0.001). The sensitivity of type I&IV to the identification of non-peripheral diseases was 78.7% (95%CI: 60.6% to 90.3%), and specificity was 98.5% (95%CI: 91.3% to 99.9%).

We compared the diagnostic performance of three strategies (B-vHIT, HINTS, and the combination of B-vHIT and HINTS) for distinguishing non-peripheral vertigo and peripheral vertigo. HINTS alone demostrated a sensitivity of 78.79% (95%CI:60.60% to 90.37%) and a specificity of 85.92% (95%CI: 75.16% to 92.69%). B-vHIT alone achieved a sensitivity of 72.72% (95% CI: 54.12% to 83.79%) and a specificity of 92.96% (95%CI: 83.65% to 97.38%). Notably, the combination of B-vHIT and HINTS exhibited synergistic enhancement in diagnostic performance: sensitivity increased to 90.91% (95% CI: 74.53% to 97.62%) and specificity remained high at 98.59% (95% CI: 91.35% to 99.92%).

5 Discussion

Vertigo is a complex neurotological disorder requiring multidisciplinary collaboration among otolaryngology, neurology, and neuropsychiatry. The overlapping symptomatology between peripheral and non-peripheral etiologies creates significant diagnostic uncertainty. Our study introduces a novel protocol leveraging B-vHIT parameters as a diagnostic indicator to differentiate between peripheral vertigo and central/ peripheral ophthalmoplegic dizziness.

The results revealed that 52% (17/33) of patients with non-peripheral vertigo exhibited reduced VOR gain in at least one semicircular canal during B-vHIT testing, which was significantly higher than previously reported in the literature^[17]. This discrepancy is mainly due to two factors. First, we did not exclude patients with various types of oculomotor palsy, as non-neurologists often have difficulty detecting subtle eye movements. We aimed to reduce the misdiagnosis rate of non-peripheral vertigo by introducing new examination indicators and assessing the application value of this new framework for acute vertigo. Second, the higher proportion of abnormal VOR gain reduction may be related to the use of binocular monitoring and the inclusion of vertical VOR analysis in our study. These findings suggest that a pathological decrease in VOR gain is not exclusively caused by peripheral vestibular disorders but may indicate lesions at any neuronal level along the vestibular pathway, particularly within the high-frequency range of the angular VOR.

Our results showed significant differences in interocular gain among the periphery vertigo group, central vertigo group, and POD group. Post-hoc comparisons indicated that, based on Asymmetry and Difference values, POD ranked highest, followed by central vertigo, then peripheral vertigo. This may be explained by the pathway mechanism of VOR. During the impulse, the head rotation deflects the cupula and bends the hair cell bundles, triggering action potentials in the primary afferents of the SCCs. These afferents project to the vestibular nuclei and subsequently to the motoneurons of the extraocular muscles, resulting in conjugate eye movements^[5, ^18]. Peripheral vestibular lesions primarily affect the VOR afferent pathway, while central injury and neuromuscular paralysis affect the VOR efferent pathway^[8].

Additionally, neuromuscular paralysis affects VOR more inconsistently than central injury does. When the neuromuscular function that governs eye movements is compromised by diseases, the precise conjugacy of eye movements may be disrupted. Previous studies have demonstrated that in patients with unilateral sixth nerve palsy, the horizontal VOR gain was reduced in both abduction and adduction of the paretic eye. Similarly, in patients with unilateral the fourth nerve palsy, the torsional, vertical, and horizontal VOR gains were reduced during incyclotorsion, depression, and abduction of the paretic eye, whereas the gains in the non-paretic eye remained normal in all directions^[19, ^20]. It should be noted that complete or partial paralysis of the ocular motor cranial nerves or their corresponding muscles, arising from diverse etiologies, can disrupt conjugate eye movement^[21, ^22]. Patients with these conditions may experience clinical manifestations such as vertigo, diplopia, blurred vision and imbalance. As described in previous studies, a disconjugate vHIT pattern between the right and left eye was observed in multiple sclerosis patients with internuclear ophthalmoplegia (INO) using the binocular scleral search coil technique^[6]. This is due to a lesion in the medial longitudinal fasciculus (MLF), which causes slowed or impaired adduction of the ipsilateral eye and abduction of the contralateral eye^[6, ^23]. In these patients, the gain values, which may vary depending on the affected site and the recorded eye of the vHIT, can be either normal or abnormal. These findings highlight the deficiencies of monocular-vHIT in patients with peripheral neuromuscular shortcoming and demonstrated the superiority of binocular vHIT, enabling timely recognition of dis-conjugated eye movements for accurate diagnosis.

In our study, we introduced two novel indicators derived from B-vHIT data: Interocular Gain Asymmetry and Interocular Gain Difference. These indicators were designed to assess the dis-conjugate eye movement. Our results confirmed that these indicators help differentiate non-peripheral from peripheral vertigo, thereby reducing misdiagnosis of central vestibular diseases and ophthalmoplegia as peripheral vertigo. We determined that an Interocular Gain Asymmetry cutoff of 16 and an Interocular Gain Difference cutoff of 0.2 were optimal for identifying non-peripheral vertigo. Our analysis revealed that there was no significant difference in Difference between the healthy group and the peripheral vertigo group, but due to the mathematical ratio, Asymmetry showed a significant difference. Therefore, we preferred to use the Difference to reflect the inconsistency of interocular gain.

By integrating Gain and Difference into our classification framework, we achieved a sensitivity of 0.79 and a specificity of 0.99 for the identification of non-peripheral diseases (Type I & IV), which were superior to monocular vHIT^[24]. By incorporating the Difference indicator, we successfully distinguished 13 patients with B-vHIT type IV from peripheral vertigo, enhancing vHIT’s sensitivity in identifying non-peripheral vertigo. Additionally, we identified 4 patients with B-vHIT type II, 2 of whom were confirmed to have cerebral infarction via brain MRI, and the other 2, with negative MRI results, were diagnosed separately with Guillain-Barré syndrome and paraneoplastic cerebellar ataxia. This indicates that a positive Difference for Interocular Gain can provide a useful clue for possibility of central lesions, especially when MRI is negative, prompting further neurological evaluation for such patients. Besides, we also found that 3 patients with B-vHIT type III couldn't be distinguished from peripheral vertigo using only B-vHIT due to combined peripheral and central vestibular involvement and near-complete extraocular muscle paralysis. Reviewing their clinical data, 2 cases of brainstem infarction and 1 case of anterior inferior cerebellar artery infarction, all of which involved of the both the peripheral and central vestibules. The involvement of the peripheral vestibules led to positive Gain (+), while the bilateral symmetrical involvement of the efferent pathways resulted in Differences (−). Another case involved vestibular nucleus infarction accompanied by gaze-evoked nystagmus. The infarction was confined to the ipsilateral vestibular nucleus, without involvement of the MLF or oculomotor nerve nucleus. The unilateral afferent nerve lesion showed a positive gain, but Different value remained normal due to the lack of binocular coordination. The last one was diagnosed as Miller-Fisher syndrome, featuring almost complete paralysis of the extraocular muscles. Because the vHIT gain in both eyes was too low to produce any difference. These findings suggest that we need to interpret it carefully and combine them with neurological examination if encountering B-vHIT results similar to such patients.

Therefore, clinicians should recognize that a negative result in both Gain and Difference or a positive result in both Gain and Difference strongly suggests non-peripheral vestibular vertigo. We suggest that the B-vHIT should be used as an alternative test to monocular vHIT in clinical settings for rapid etiological discrimination, which can influence therapeutic decision-making.

Our study has some limitations. The subgroup of central vertigo was not accurately categorized into supranuclear, internuclear and subnuclear due to the limited sample size. Another limitation of the present study is that the normative reference values for B-vHIT were established based on a healthy cohort aged 20–40 years, which may not fully reflect the physiological changes in VOR function associated with aging. The elderly patients in the vertigo diseases group may experience changes in binocular Gain parameters due to the aging-related degenerative changes. Future studies should enroll healthy participants across a broader age spectrum to establish age-stratified normative data, which would enhance the clinical applicability of B-vHIT across diverse age groups.

6 Conclusions

The application of B-vHIT, a novel classification framework integrating Gain and Difference of Interocular Gain, significantly distinguish between peripheral and non-peripheral causes of acute vertigo. Utilizing the Gain and Difference obtained from the B-vHIT would aid in the detection and localization of potential lesions involving the VOR pathway and eye muscles. Furthermore, the optimal cutoff values can further contribute to improving the diagnostic accuracy for determining the etiology of vertigo

References

[1] Tarnutzer AA , Berkowitz AL , Robinson KA , Hsieh YH , Newman-Toker DE . Does my dizzy patient have a stroke? A systematic review of bedside diagnosis in acute vestibular syndrome. CMAJ, 2011, 183(9): E571–592

[2] Murphy C , Reinhardt C , Linehan D , Katiri R , O'Connor A . A review of primary care referrals for patients with dizziness and vertigo: prevalence and demographics. Ir J Med Sci, 2022, 191(1): 385–389

[3] Gerlier C , Hoarau M , Fels A . et al. Differentiating central from peripheral causes of acute vertigo in an emergency setting with the HINTS, STANDING, and ABCD2 tests: A diagnostic cohort study. Acad Emerg Med, 2021, 28(12): 1368–1378

[4] Robinson DA . Signal processing in the vestibulo-ocular reflex. Prog Brain Res, 2022, 267(1): 169–181

[5] Welgampola MS , Taylor RL , Halmagyi GM . Video Head Impulse Testing. Adv Otorhinolaryngol, 2019, 82: 56–66

[6] Aw ST , Chen L , Todd MJ , Barnett MH , Halmagyi GM . Vestibulo-ocular reflex deficits with medial longitudinal fasciculus lesions. J Neurol, 2017, 264(10): 2119–2129

[7] Choi JY , Lee SH , Kim JS . Central vertigo. Curr Opin Neurol, 2018, 31(1): 81–89

[8] BeryAKHongYCKuoYHChangTP. Vestibulo-Ocular Reflex Dysconjugacy Associated With Central Cause of Dizziness. Ear Hear. 2025;46(5):1247–1253.

[9] Kim SH , Kim HJ , Kim JS . Isolated vestibular syndromes due to brainstem and cerebellar lesions. J Neurol, 2017, 264(Suppl 1): 63–69

[10] Choi SY , Kee HJ , Park JH , Kim HJ , Kim JS . Combined peripheral and central vestibulopathy. J Vestib Res, 2014, 24(5-6): 443–51

[11] Bery AK , Chang TP . Positive horizontal-canal head impulse test is not a benign sign for acute vestibular syndrome with hearing loss. Front Neurol, 2022, 13: 941909

[12] Lee SH , Kim JS . Differential diagnosis of acute vascular vertigo. Curr Opin Neurol, 2020, 33(1): 142–149

[13] Choi JY , Kim HJ , Kim JS . Recent advances in head impulse test findings in central vestibular disorders. Neurology, 2018, 90(13): 602–612

[14] Newman-TokerDEKattahJCAlverniaJEWangDZ. Normal head impulse test differentiates acute cerebellar strokes from vestibular neuritis. Neurology. 2008;70(24 Pt 2):2378–2385.

[15] Wettstein VG , Feil B , Mono ML . Case report: A disconjugate pattern in video head impulse testing hints toward a central cause of acute vertigo. Front Neurol, 2023, 14: 1222475

[16] Thomas JO , Sharobeam A , Venkat A . et al. Video head impulse testing to differentiate vestibular neuritis from posterior circulation stroke in the emergency department: a prospective observational study. BMJ Neurol Open, 2022, 4(1): e000284

[17] Ha SH , Lee DK , Park G . et al. Prospective analysis of video head impulse tests in patients with acute posterior circulation stroke. Front Neurol, 2023, 14: 1256826

[18] Halmagyi GM , Chen L , MacDougall HG , Weber KP , McGarvie LA , Curthoys IS . The Video Head Impulse Test. Front Neurol, 2017, 8: 258

[19] Wong AM , Sharpe JA , Tweed D . The vestibulo-ocular reflex in fourth nerve palsy: deficits and adaptation. Vision Res, 2002, 42(18): 2205–2218

[20] Wong AM , Tweed D , Sharpe JA . Adaptations and deficits in the vestibulo-ocular reflex after sixth nerve palsy. Invest Ophthalmol Vis Sci, 2002, 43(1): 99–111

[21] Frohman EM , Frohman TC , O'Suilleabhain P . et al. Quantitative oculographic characterisation of internuclear ophthalmoparesis in multiple sclerosis: the versional dysconjugacy index Z score. J Neurol Neurosurg Psychiatry, 2002, 73(1): 51–55

[22] Kim SH , Zee DS , du Lac S , Kim HJ , Kim JS . Nucleus prepositus hypoglossi lesions produce a unique ocular motor syndrome. Neurology, 2016, 87(19): 2026–2033

[23] Lee SH , Kim JM , Kim JS . Update on the medial longitudinal fasciculus syndrome. Neurol Sci, 2022, 43(6): 3533–3540

[24] Machner B , Erber K , Choi JH , Trillenberg P , Sprenger A , Helmchen C . Usability of the head impulse test in routine clinical practice in the emergency department to differentiate vestibular neuritis from stroke. Eur J Neurol, 2021, 28(5): 1737–1744

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