key: cord-0946523-l58698zo authors: Mantokoudis, Georgios; Otero-Millan, Jorge; Gold, Daniel R. title: Current concepts in acute vestibular syndrome and video-oculography date: 2021-12-09 journal: Curr Opin Neurol DOI: 10.1097/wco.0000000000001017 sha: bc0111a418a8a55daf7e67ec0f4414dc7435e71e doc_id: 946523 cord_uid: l58698zo PURPOSE OF REVIEW: We present here neuro-otological tests using portable video-oculography (VOG) and strategies assisting physicians in the process of decision making beyond the classical ‘HINTS’ testing battery at the bedside. RECENT FINDINGS: Patients with acute vestibular syndrome (AVS) experience dizziness, gait unsteadiness and nausea/vomiting. A variety of causes can lead to this condition, including strokes. These patients cannot be adequately identified with the conventional approach by stratifying based on risk factors and symptom type. In addition to bedside methods such as HINTS and HINTS plus, quantitative methods for recording eye movements using VOG can augment the ability to diagnose and localize the lesion. In particular, the ability to identify and quantify the head impulse test (VOR gain, saccade metrics), nystagmus characteristics (waveform, beating direction and intensity), skew deviation, audiometry and lateropulsion expands our diagnostic capabilities. In addition to telemedicine, algorithms and artificial intelligence can be used to support emergency physicians and nonexperts in the future. SUMMARY: VOG, telemedicine and artificial intelligence may assist physicians in the diagnostic process of AVS patients. The acute vestibular syndrome (AVS), first introduced by Hotson and Baloh [1] , consists of a continuous state of dizziness (>24 h), nystagmus, gait disturbance, nausea, vomiting and motion intolerance [2, 3] . The classification into episodic, acute and chronic vestibular syndromes was driven forward by the international committee of the Barany Society and is now reflected in the new ICD-12 catalogue of the WHO. Subcategories for the AVS have recently been described, including spontaneous and triggered AVS [4] . A previous approach focused on symptoms and risk stratification rules, which was associated with a high rate of misdiagnosis [5, 6] . Even neuroimaging (MRIs) in the acute state miss about 20-50% of causes of AVS (such as strokes) [7] and is not cost and time-efficient if applied to all AVS patients. Therefore, current concepts suggest a targeted history (including questions about timing and triggers) [4] and a clinical examination focusing on eye movements [8] . The bedside 'HINTS' examination (head impulse test, nystagmus, test of skew) was first introduced in 2009 by Kattah et al. [9] , and in the hands of subspecialists, has a higher sensitivity and specificity to detect a central cause of the AVS as compared to MRI. Recent literature recommends the use of video-oculography (VOG) in order to record and quantify nystagmus and the vestibulo-ocular reflex (VOR, using video head impulse test) when possible. Quantification of eye movements compared with a clinical examination using Frenzel glasses has the following advantages: (1) It is less dependent on the clinical skills of the examiner. (2) It is cost-efficient compared with neuroimaging. (3) It allows for subtle nystagmus to be more easily appreciated. (4) It allows an automated analysis of test results, and finally (5) recording the examination makes it possible for a subspecialist to review remotely. This review intends to present current concepts in the clinical assessment and diagnostic work-up of patients with the AVS using VOG and modern algorithms in eye movement detection. AVS accounts for nearly 20-25% of dizzy patients visiting the emergency department (ED). Of the AVS patients, 20-25% will have a cause that is potentially life-threatening such as posterior fossa stroke. The large spectrum of diseases causing AVS (Table 1) makes it difficult for a physician to identify the patient at risk using the history and risk stratification alone. Table 1 summarizes a list of differential diagnosis causing an AVS. 'HINTS' has a high sensitivity and specificity [2, [9] [10] [11] in detecting vestibular strokes, which exceeds that of the acute MRI performed within 24-48 h after symptom onset [2, 12] . Strokes smaller than 1 cm can be missed in up to 50% of the cases within the first 24 h [7] . 'HINTS' allows a fast and accurate bedside assessment of AVS patients even without Frenzel glasses; however, its accuracy is highly dependent on the examiner's experience. The sensitivity and specificity of 'HINTS' performed by nonexperts is not clearly known. In addition, the sensitivity of 'HINTS' is reduced if AVS patients do not present with spontaneous nystagmus. It was shown that nonexperts (e.g. emergency physicians) used 'HINTS' on almost all dizzy patients regardless the underlying syndrome or the presence of nystagmus [13] . Nystagmus might serve as a biomarker for the severity of symptoms, mandatory for the application of the 'HINTS' examination. Unpublished data from a larger cross-sectional study revealed that 50% of dizzy stroke patients did not have spontaneous nystagmus even after removal visual fixation [14 && ]. It is under debate, whether we should consider spontaneous nystagmus as a mandatory feature for the classification of AVS. Another clinical feature, such as postural or gait stability, could serve as another 'marker' of severity and predict stroke [15] . The video head impulse test (vHIT) is the most potent test to detect a vestibular stroke with an estimated sensitivity of 88% and specificity of 92% [11] . Although experts might perform HITs at the bedside accurately, the assessment (or interpretation) of a clinical HIT without the support of VOG remains difficult due to spontaneous nystagmus and covert corrective saccades [16] . vHIT allows for quantification of the VOR, including gain measurements of the slow phase of the VOR and fast phase metrics such as saccade latencies and amplitude. It was found that VOR gain cutoff more than 0.68 for lateral (horizontal) vHIT was predictive for stroke [11, 17, 18] . vHIT gain is normal in most PICA strokes but can be unilaterally or bilaterally abnormal in AICA strokes [11] . VOR gain asymmetry less than 20% (absolute asymmetry) or less than 8-10% (Jongkees formula using a normalization procedure) was predictive as well [18] . Further saccade analysis such as cumulative saccade amplitude could further increase the accuracy of stroke prediction [19] ; however, this study was performed with scleral search coils and confirmation of study results using vHIT is still lacking. vHIT is prone to artifacts similar to any other eye tracking based system [20] . The results collected with VOG/vHIT are operator-dependent, although the quality of data can be enhanced and artifacts minimized through training. In fact, we observed a steep learning curve and significant improvement in performance after exceeding 160 HITs [21] . There is no need for a large head excursion with vHIT as is typically necessary with the clinical HIT; however, most of the vHIT operators struggle to KEY POINTS VOG and video head impulse test-enhanced HINTS examination allows a quantification of eye movements, including additional features beyond the classical HINTS examination. Nonexperts might benefit from a standardized battery of eye movement tests in conjunction with telemedicine offered by subspecialists. Quantification of eye and head movements would enable future automated analysis. perform the movements at high enough head accelerations. Artifacts might still occur even in the hands of an experienced examiner; however, there is no major impact of artifacts on the final result as long as the number of valid vHITs is larger than 10-20 trials [22] . Although the various vHIT systems calculate VOR gain differently, there is no superiority in the method used provided that the vHITs are properly recorded [23] . Nystagmus can be recorded using current VOG devices. vHIT devices record eye position traces at higher frame rates (>200/s); however, binocular recordings are often not possible, as the devices must be lightweight enough for dynamic tests such as vHIT. Testing gaze holding with vHIT can be achieved either by maintaining eccentric gaze focusing on the examiner's fingers (nonstandardized gaze angle) or on a visual target projected either on a wall, screen or led light on the goggles frame (standardized gaze angle). Although nystagmus and nystagmus-like eye movements have been recently classified by the international consensus committee of the Bárány Society [24 && ], the evaluation of nystagmus in 'HINTS' includes only a qualitative assessment of beating direction of horizontal nystagmus in primary and eccentric gaze in light. Nystagmography offers additional quantitative parameters including its slow phase 'waveform', which is one metric that can be used to distinguish a peripheral from a central lesion in AVS patients. For example, a patient with a stroke can have gaze-evoked nystagmus with a decreasing slow phase velocity waveform ( Fig. 1a) , whereas a patient with vestibular neuritis will have (vestibular) nystagmus with a linear slow phase velocity waveform ( Fig. 1b) [25] . Gaze-evoked nystagmus can often be asymmetric with a more intense nystagmus towards one gaze direction. These patients often have a spontaneous nystagmus at straight gaze as well with a shift of their 'null point', which is a gaze position wherein no eye drift occurs ( Fig. 1a ) [26 & ], which is similar to 'Bruns' nystagmus (e.g. cerebellopontine angle tumour or certain posterior fossa syndromes). When present, Bruns nystagmus may allow for determination of the lesion side, for example gaze-evoked nystagmus is typically ipsilesional and vestibular nystagmus is typically contralesional [26 & ]. It has also been demonstrated that patients with the AVS due to stroke have lower intensity nystagmus (<128/s) compared with patients with an acute unilateral vestibulopathy [14 && ]. Although traditional teaching was that spontaneous nystagmus due to an acute peripheral vestibulopathy should be suppressed or partially suppressed by visual fixation, fixation often suppresses spontaneous nystagmus due to stroke as well. However, the magnitude of suppression is lower in stroke patients compared with those with vestibular neuritis [14 && ]. A reduction in nystagmus of less than 28/s in light (using VOG) is predictive of stroke [13] . However, such subtle changes could be easily overlooked on bedside examination, although the absence or presence (and to what degree) of fixation suppression can be clinically useful. A vertical ocular misalignment, or skew deviation, can be seen in both peripheral [27] and central causes of AVS, as lesions at various levels of the otolithic (utricular) pathway may lead to an ocular tilt reaction (OTR), including head tilt, ocular counterroll and skew. Typical central lesions producing pathologic OTR occur in the vestibular nuclei (lateral medullary or Wallenberg syndrome, caudal to the decussation of utriculo-ocular motor fibres causing an ipsiversive OTR), medial longitudinal fasciculus (usually pontine -rostral to the decussation causing a contraversive OTR) and the interstitial nucleus of Cajal (midbrain -contraversive OTR) [28] . A recent cross-sectional study of AVS patients found a skew deviation prevalence of 26% [29] ; however, this included some very small skews that were detected only with VOG and not with bedside ocular alignment testing. Skews larger than 3.3 degrees (5.8 diopters) were indicative of stroke and typically caused vertical diplopia, while 'peripheral' skews were smaller in magnitude and rarely caused vertical diplopia. Because the very small 'peripheral' skews could not be appreciated in these studies without VOG or Maddox rod testing, alternate cover testing as part of the originally described HINTS examination ('Test of Skew') was sufficient to recognize larger skews (>3 degrees) that were likely to be central in origin. We observed a difficulty in recording skew with VOG due to the following reasons: (1) Small skews are not detectable in noisy signals due to artifacts or improper eye tracking. (2) There can be a lack of synchronization between visual stimulus (right versus left eye viewing occurring during alternate cover) and the detection of saccades in time dependency of the stimulus. (3) There might be an overestimation of skew in patients with spontaneous nystagmus with a vertical component or a potential crosstalk between horizontal and vertical eye movements. Crosstalk occurs when we observe simultaneous and synchronous vertical eye movements (refixation movements during alternate cover) during pure horizontal eye movements (spontaneous horizontal nystagmus). It can be the result of an improper head/eye calibration when VOG goggles or the cameras on the head are tilted. A classical pipeline of automatic nystagmus analysis starts with raw eye position recordings obtained with any VOG or eye tracking device [30] . The ultimate objective is to classify the recording into categories of interest, for example into nystagmus present or absent or into nystagmus that is pathological or physiological. To accomplish this, there are several necessary steps to analyse the data (Fig. 2) . First, data must be cleaned of blinks and other artifacts that may appear in the data, for example due to errors in tracking. If not properly removed, these artifacts may produce spurious instances of apparent high slow-phase velocity and potentially cause a misclassification of the recording. Second, different portions of the eye movement recording need to be identified. Although quickphases do relate to nystagmus intensity, we often focus the analysis on the slow-phases, as they more directly correspond with vestibular sensation and vestibular neural pathways. Thus, the analysis must identify the slow phases within the recordings and eliminate the quick phases. Other portions that may need to be removed are periods of time when the head is actually moving, as slow phases will appear as part of the normal vestibular ocular reflex of the individual. Third, after data are cleaned and segmented, it is usually desirable to obtain an estimation of the instantaneous slow-phase velocity. This signal will measure the intensity of the nystagmus over time with a temporal precision ideally between a few hundred milliseconds to one second. From this signal, the relevant features for classification can be calculated such as maximum slow-phase velocity, mean slow-phase velocity, time to peak and so on. The relevant features will vary depending on the particular test being analysed. For example, during gaze testing, we may just be interested in mean slowphase velocity during the entire recording, but during a positional test such as the Dix Hallpike manoeuvre, we want to capture the characteristics of the temporal evolution of the signal, that is how fast it raises, how fast it decays and if it ever changes direction. Finally, in the simplest case, recordings will be classified according to a threshold and a single feature. For example, whether or not the maximum slow-phase velocity is above a particular speed such as 5 or 10 degree/s. In a more complicated example, we may want to use several features to determine whether the waveform corresponds with a typical crescendo and decrescendo nystagmus waveform from benign paroxysmal positional vertigo (BPPV) during positional testing. With the advent of machine learning, these steps can be combined into a single machine learning instance that is trained to directly classify eye movement recordings [31] . However, there are two steps that need to occur prior to trying to classify any new recording. First, a large dataset must be collected and labelled by a set of experts. This labelling must correspond with the indented classification to be performed by the machine. For example, a recording in a dataset could be labelled as having nystagmus present or absent according to the experts. Then, the machine is trained with this dataset and becomes ready to classify new recordings. In some cases, machine learning may be used to directly diagnose the patient by combining results and features obtained from multiple tests [32 && ]. In others, machine learning can be used to only replace an individual step or group of steps in the classical analysis pipeline. For example, machine learning could be used to detect and remove the quick phases in the recordings. Multiple machine learning methods have been developed to detect saccades, which is a similar problem to quick-phase detection. But as shown in a recent study, they will fail in detecting quick-phases of nystagmus because their model was trained with data wherein the eye was relatively still in between saccades [33] . It may be also relevant to compare the challenges of analysing nystagmus versus head impulse tests. One could argue that nystagmus is easier to analyse by the human eye than by a machine, while the opposite is true for head impulse test. Nystagmus data collection is typically done just once, if something goes wrong and data are contaminated by artifacts it may be hard to recover the relevant features or measurements. In the HIT, on the contrary, an expert can select the appropriate times to do each impulse and coordinate with the individual to have the eyes open and optimize the quality of the data thus minimizing the chance of artifacts. Moreover, data from all impulses are averaged, further reducing the effect of noise or artifacts in single impulse. Nystagmus can be evaluated clinically and qualitatively either by looking at the patients' eyes, videos or raw eye position traces. Artifacts that are easily ignored by the expert eye can be a challenge for the automatic processes. On the contrary, for HIT, it is easier for the computer algorithms to precisely determine the result by measuring either gain or catch-up saccade frequency, although the clinical assessment must rely exclusively on the presence of catch-up saccades. This reliance in subjective assessment of nystagmus may have resulted in a reduced number of studies analysing the data quality and effect of artifacts in automatic nystagmus analysis while they have been carefully studied for HIT [22] . As we move towards more automated analysis of nystagmus, the lack of input from an expert to identify artifacts or problems with the recording must be recognized as new algorithms are developed and refined. 'HINTS' plus includes a fourth step, which is intended to diagnose acute hearing loss in AVS patients [10] . Hearing is often tested with finger rubbing at the bedside [10, 34, 35] , although this test has a low specificity since the produced sound pressure level is very low (<60 dB SPL). Audiometric assessment under controlled conditions, however, are often not available in EDs. Hearing loss and simultaneous vestibular loss could be the result of an inner ear inflammation such as a labyrinthitis in 50-60% of AVS patients. These inflammatory conditions are assumed to arise from viral or postviral causes akin to patients presenting with isolated loss of vestibular (i.e. vestibular neuritis) or auditory (i.e. idiopathic sudden sensorineural hearing loss) function. In these cases, otoscopy is typically normal unless there is an underlying infection such as an otitis media. The range of hearing loss severity is often variable from mild to severe or even complete deafness. However, hearing loss might also be a red flag due to involvement of the anterior inferior cerebellar artery (AICA, pontine structures including the cochlear nucleus and the nerve entry zone -this is rare) and the internal auditory artery (a branch of the AICA causing labyrinthine ischemia, this is much more common) [36] . Different patterns and severity of hearing loss can be classified by audiometric testing [36] . Interestingly, there is a high recovery rate reported [37] . A moderate to severe hearing loss (>70 dB) on all frequencies would be expected due to cochlear infarction, which in fact has been demonstrated with MRI-proven posterior circulation infarctions [37] . We would further expect an isolated high frequency loss if there is isolated involvement of the vestibulocochlear artery and the cochlear ramus supplying the basal turn of the cochlea. Such isolated small emboli would not be visible in current imaging modalities and occur often after decompression sickness. Further studies quantifying hearing loss are needed in order to develop and recommend any quantitative screening tool for hearing loss in the future. A recent study proposed another bedside test to apply in patients with the AVS, looking for evidence of ocular lateral deviation (lateropulsion) [38 & ]. Ocular lateral deviation is a conjugate horizontal deviation occurring under closed eyelids, which has been shown to be present in 12% of stroke patients presenting with the AVS. Patients are asked to close their eyes for 3-5 s, and when opening the eyes, the examiner should look for corrective eye movements (saccades) back towards the centre. Ocular lateral deviation is most commonly seen in a lateral medullary (Wallenberg) syndrome, wherein saccades are typically hypermetric towards the lesion and hypometric away from the lesion. Under closed eyelids, ocular deviation occurs toward the side of the lesion (known as ipsipulsion), and when the eyes are opened, contralesional hypometric saccades will bring the eyes back to centre. This test showed a low sensitivity of 12% but a specificity of 100% for a central lesion [38 & ], but when present, is highly suggestive of a central lesion. In the hands of eye movement experts, HINTS is proven. However, its sensitivity and specificity in the hands of nonsubspecialists is unknown. Although dizziness/vertigo is a common complaint in the ED, there are few subspecialists to evaluate these patients. So, how can we utilize VOG/vHIT technology in the ED where getting the diagnosis wrong can be life-threatening? Implementation of a 'tele-dizzy' clinical service that includes a standardized battery of VOG tests (mainly HINTS and Dix-Hallpike/supine roll) would enable a single expert to drastically expand their clinical reach through simultaneous coverage of multiple EDs. A tele-dizzy service could reliably, inexpensively and quickly distinguish ear and brain causes of dizziness and vertigo, as experts are providing the interpretation. Eye movement specialists can now almost instantaneously review a VOG examination remotely in minutes, enabling rapid tele-diagnosis. Addition of a standardized dizzy questionnaire would enhance localization and the ability to generate an accurate differential diagnosis, especially in patients with transient symptoms or in those without spontaneous nystagmus wherein HINTS cannot be applied. A tele-dizzy service would enable standard expert clinical care provided by a remote means. In fact, at The Johns Hopkins Hospital, 290 teledizzy consults have been performed since 2017 with a drastic measurable increase in diagnostic yield and decrease in unnecessary test utilization compared with a baseline ED population. The rate of specific vestibular diagnoses made in the ED with tele-dizzy is 57% compared with a baseline rate of 21% (þ176%). Furthermore, our tele-dizzy service has recommended computed tomography (CT) scans 2% of the time compared to a baseline CT rate of 49% (-96%). Next steps include scaling this consultation service for expansion to other hospitals. We also see an important role for smartphone app VOG-based triage from home in the future. This would allow for the accurate diagnosis of BPPV, but could also detect red flag signs (e.g. spontaneous vertical/vertical-torsional nystagmus; vertical refixation with test of skew) that would prompt rapid referral to the ED. The systematic use of VOG devices is a first step in the process of quantification and objective classification of clinical signs in AVS patients such as abnormal head impulses, spontaneous nystagmus, skew, pathologic saccade metrics and other eye movements. There is, however, a lack of an automated VOG interpretation. We suggest a similar approach to that seen in patients with acute chest pain and suspected heart attack. A point-of-care examination such as an ECG performed by nonexperts in the ED allows an automated computerized ECG interpretation. Analogous to an ECG, an automated VOG exam in conjunction with artificial intelligence could pave the way for a broadly available decision support system. There is no doubt that the HINTS examination is highly effective in detecting central causes of the AVS in the hands of subspecialists. Dissemination of the HINTS examination is still limited in nonsubspecialists, perhaps due to its absence in medical school and residency programme curriculums, or that its importance is under-emphasized for neurology, otolaryngology and emergency medicine trainees. When the HINTS examination is performed by nonsubspecialists, it is commonly applied incorrectly (e.g. HINTS examination in a patient with positional vertigo), performed incorrectly (e.g. the HIT) or interpreted incorrectly (e.g. a 'peripheral' HINTS is diagnosed in a patient who actually has a stroke). Ideally, the HINTS examination would always be performed by a subspecialist, although this is practically impossible due to a paucity of eye movement/vestibular experts. A battery of recorded VOG/vHIT testing in the emergency setting using a store-and-forward methodology (akin to a radiologist reading a study) would allow for one expert to remotely review and interpret patient data from multiple locations. Practically speaking, leveraging technology in this way allows the subspecialist to participate in the care of the patient early in their course with benefits, including decreasing (unnecessary) test utilization, and increasing diagnostic accuracy (see 'AVS and telemedicine' section above). However, even subspecialists may struggle to distinguish central from peripheral causes in select cases. As discussed above, there are quite a few caveats and exceptions to the HINTS examination rules, and VOG/vHIT can be a powerful tool to enhance diagnostic accuracy. (1) Head impulse test -there are a variety of central localizations and stroke syndromes that are capable of producing an abnormal HIT. Video HIT allows for quantification of the gain, and the lower the gain, the greater the likelihood that a peripheral vestibulopathy is the culprit. The function of all six semicircular canals can be quantified with vHIT, allowing for identification of superior (horizontal and anterior canal) and/or inferior (posterior canal) vestibular nerve involvement. (2) Nystagmus -with VOG, slow phase velocity waveforms can be analysed; subtle changes in slow phase velocity can be measured in fixation and fixation-removed conditions (greater suppression with fixation in peripheral vestibulopathy); horizontal, vertical, torsional components of nystagmus can be analysed and quantified. (3) Test of skew -with VOG, small skews that are not enough to cause diplopia may be detected, which could be helpful for the subspecialist (who can localize and diagnose a 'peripheral' skew due to utricle involvement in vestibular neuritis). Acute VOG/vHIT testing in the emergency room has the potential to revolutionize the care of dizzy patients. The VOG/vHIT-enhanced HINTS examination has many benefits over the clinical/bedside HINTS, but perhaps most importantly it would allow a single subspecialist to impact many patients due to remote review and interpretation capabilities. The development of algorithms would enable further scalability through rapid automated diagnosis of the clearly benign (e.g. BPPV, peripheral vestibulopathy) and dangerous (e.g. stroke) disorders, allowing the subspecialist to focus in on the most challenging and ambiguous cases. We believe that VOG/vHITbased diagnosis and triage of acutely dizzy patients should be (and will be) the standard of care, although a variety of technological, logistical and financial/billing barriers must first be surmounted. Acute vestibular syndrome Does my dizzy patient have a stroke? A systematic review of bedside diagnosis in acute vestibular syndrome Use of HINTS in the acute vestibular syndrome. An overview TiTrATE: a novel, evidence-based approach to diagnosing acute dizziness and vertigo Disconnect between charted vestibular diagnoses and emergency department management decisions: a cross-sectional analysis from a nationally representative sample Overreliance on symptom quality in diagnosing dizziness: results of a multicenter survey of emergency physicians Small strokes causing severe vertigo: frequency of false-negative MRIs and nonlacunar mechanisms Diagnosing stroke in acute vertigo: the HINTS family of eye movement tests and the future of the HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging HINTS outperforms ABCD2 to screen for stroke in acute continuous vertigo and dizziness VOR gain by head impulse video-oculography differentiates acute vestibular neuritis from stroke Vertigo and hearing loss Diagnostic accuracy of the HINTS exam in an emergency department: a retrospective chart review Stroke prediction based on the spontaneous nystagmus suppression test in dizzy patients: a diagnostic accuracy study The authors of this prospective cross-sectional study demonstrated in 84 patients with an acute vestibular syndrome that nystagmus suppression (recorded with VOG) was decreased in stroke patients compared with patients with vestibular neuritis The diagnostic accuracy of truncal ataxia and HINTS as cardinal signs for acute vestibular syndrome How good are we in evaluating a bedside head impulse test? Paradigm shift in acute dizziness: is caloric testing obsolete? Quantitative video-oculography to help diagnose stroke in acute vertigo and dizziness: toward an ECG for the eyes Head impulse gain and saccade analysis in pontine-cerebellar stroke and vestibular neuritis Quantifying the vestibuloocular reflex with video-oculography: nature and frequency of artifacts Quantifying a learning curve for video head impulse test: pitfalls and pearls Impact of artifacts on VOR gain measures by video-oculography in the acute vestibular syndrome VOR gain calculation methods in video head impulse recordings Classification of vestibular signs and examination techniques: nystagmus and nystagmus-like movements This study presents a comprehensive classification and definitions for types of nystagmus provided by the international classification committee of the Bá rá ny Society The neurology of eye movements Bruns' nystagmus revisited: a sign of stroke in patients with the acute vestibular syndrome The authors studied gaze evoked nystagmus in 47 patients with an acute vestibular syndrome and 64 healthy individuals. They present special nystagmus patterns recorded with VOG HINTS Examination in Acute Vestibular Neuritis: Do Not Look Too Hard for the Skew Vestibular syndromes in the roll plane: topographic diagnosis from brainstem to cortex Acute vestibular syndrome: is skew deviation a central sign? Automatic nystagmus detection and quantification in long-term continuous eye-movement data 1D convolutional neural networks for detecting nystagmus Modern machine-learning can support diagnostic differentiation of central and peripheral acute vestibular disorders Such an approach could pave the way for a widespread use of artificial intelligence in order to support diagnostic decisions at the bedside Automatic quick-phase detection in bedside recordings from patients with acute dizziness and nystagmus Update on HINTS Plus, with discussion of pitfalls and pearls Symptoms and signs of neuro-otologic disorders Audiovestibular loss in anterior inferior cerebellar artery territory infarction: a window to early detection? Sudden deafness in vertebrobasilar ischemia: clinical features, vascular topographical patterns and long-term outcome Ocular lateral deviation with brief removal of visual fixation differentiates central from peripheral vestibular syndrome Ocular lateral deviation is a simple, but highly specific bedside test for stroke localization and lateralization Intracranial vertebral artery dissection mimicking acute peripheral vertigo Prolonged dysphagia due to Listeriarhombencephalitis with brainstem abscess and acute polyradiculoneuritis Acute vestibular paralysis in herpes zoster oticus Mumps virus may damage the vestibular nerve as well as the inner ear Neuroborreliosis in the etiology of vestibular neuronitis Acute unilateral peripheral vestibulopathy in neurosyphilis A case series of vestibular symptoms in positive or suspected COVID-19 patients Vestibular Neuritis as Clinical Presentation of COVID-19 Vestibular neuritis caused by severe acute respiratory syndrome coronavirus 2 infection diagnosed by serology: Case report Vertigo as the first sign of chronic myeloid leukemia: a case report and literature review Isolated acute vestibular syndrome due to presumed primary central nervous system lymphoma involving the dorsal medulla Má rmol-Szombathy I, Domínguez-Durá n E. Paraneoplastic acute vestibular syndrome: what, when and how Vestibular neuronitis in a vestibular schwannoma patient Metastasis to the temporal bone may cause acute peripheral vestibular syndrome and impaired hearing Pé rez-Ferná ndez N. Recent onset disequilibrium mimicking acute vestibulopathy in early multiple sclerosis Multiple sclerosis as a cause of the acute vestibular syndrome Acute vestibular syndrome and hearing loss mimicking labyrinthitis as initial presentation of multiple sclerosis Vestibular signs of thiamine deficiency during the early phase of suspected Wernicke encephalopathy An unusual stroke-like clinical presentation of Creutzfeldt-Jakob disease: acute vestibular syndrome Acute vestibular syndrome in a patient with cerebral autosomal dominant leukoencephalopathy with subcortical infarcts and leukoencephalopathy (CADASIL) Acute vestibular syndrome associated with anti-GQ1b antibody Acute simultaneous bilateral vestibulocochlear impairment in neuro-Behçet's disease: a case report Audiovestibular manifestations of the antiphospholipid syndrome Cogan's syndrome: acute vestibular and auditory dysfunction with interstitial keratitis A case of bilateral internal auditory canal osteomas Superior canal dehiscence reveals concomitant unilateral utricular loss (UUL) Medullary cavernous malformation as a cause of isolated acute vestibular syndrome Acute peripheral vestibular deficits after whiplash injuries Cerebellar infarction presenting as inner ear decompression sickness following scuba diving: a case report The authors thank Dr. Athanasia Korda and Dr. Ewa Zamaro for her contribution to the VOG data of AVS patients. They also thank Dr. David Newman-Toker and Dr. Susan Peterson for their invaluable contributions to the 'Tele-Dizzy' program.Financial support and sponsorship G.M. was supported by the Swiss National Science Foundation #320030_173081. None of the investigators has any relevant financial interests, activities, relationships or affiliations that represent a relevant financial conflict of interest with respect to this article. Papers of particular interest, published within the annual period of review, have been highlighted as: & of special interest && of outstanding interest