Predictors of Chronic Dizziness in Acute Unilateral Vestibulopathy: A Longitudinal Prospective Cohort Study.

OBJECTIVE: Chronic dizziness after acute unilateral vestibulopathy (AUVP) causes significant social and economic burdens. This study aims to identify predictors of chronic dizziness. STUDY DESIGN: Prospective, longitudinal cohort study. SETTING: ENT departments from secondary and tertiary hospitals. METHODS: Participants meeting the Barany Society's diagnostic criteria for AUVP were included. Evaluations occurred within 0 to 21 days (T1), and at 4 (T2) and 10 weeks (T3) postonset. The primary outcome measure was the Dizziness Handicap Inventory (DHI) at 6 months, with a score >30 indicating chronic dizziness. Five clusters of predictors were assessed at T1-3: central vestibular compensation, visual dependence, movement exposure, psychological factors, and balance performance. Separate linear regression models for T1, T2, and T3 were constructed to explain the variability in the 6-month DHI score. Receiver operating characteristics analyses were conducted to predict chronic dizziness. RESULTS: From June 2021 to January 2024, 103 participants (55.2 ± 16.6 years old, 49 women) were included. The regression models explained the variability in the 6-month DHI score by 33.0% at T1, 47.6% at T2, and 64.0% at T3 (P < .001), including psychological factors (T1, T2, T3), visual dependence (T2, T3), and static balance performance (T3). Cutoff values for the Vestibular Activities Avoidance Instrument (23/54), Visual Vertigo Analog Scale (33.5/100), and Hospital Anxiety and Depression Scale-Anxiety (7.5/21) at 10 weeks postonset predicted chronic dizziness. CONCLUSION: Higher psychological burden, increased visual dependence, and poorer static balance performance were associated with chronic dizziness. Cutoff values were determined to identify individuals with AUVP at risk for chronic dizziness.

Altered thalamus functional connectivity in patients with acute unilateral vestibulopathy: a resting-state fMRI study.

Objective: Acute unilateral vestibulopathy (AUVP) is the second leading cause of peripheral vestibular vertigo. Full recovery of AUVP is related to sufficient central vestibular compensation. It has been confirmed that the vestibular nucleus and vestibular cortex are involved in the process of vestibular compensatory in AUVP patients. However, few studies have focused on the functional compensation of thalamus in patients with AUVP. This study aimed to explore the alterations of resting-state functional connectivity (FC) focused on thalamus using functional magnetic resonance imaging (fMRI) in AUVP patients. Methods: Data of 3D-T1 and resting-state fMRI were collected from 40 AUVP patients and 35 healthy controls (HC). Seeds-based (bilateral thalamus) FC was analyzed to investigate the changes in FC between the two groups. Furthermore, we evaluated the associations between altered thalamus FC and clinical features in AUVP patients using Pearson's partial correlation. Results: Compared with HC, AUVP patients showed decreased FC between bilateral thalamus and left insula. We also observed decreased FC between right thalamus and left supramarginal gyrus. Additionally, we found increased FC between left thalamus and right postcentral gyrus (PCG), as well as increased FC between right thalamus and regions of bilateral PCG, right middle frontal gyrus and right middle occipital gyrus in AUVP patients. Furthermore, the FC between left thalamus and left insula was negatively correlated with values of canal paresis in patients with AUVP (p = 0.010, r = -0.434). Conclusion: Our results provided first evidence for the decreased thalamo-vestibular cortex pathway, as well as increased thalamo-somatosensory and thalamo-visual cortex pathway in AUVP patients. These findings help us better understand the underlying mechanisms of central dynamic compensatory following an acute unilateral peripheral vestibular damage.

Application of a Video Head Impulse Test in the Diagnosis of Vestibular Neuritis.

In patients presenting in the emergency department with acute vertigo, a rapid and accurate differential diagnosis is crucial, as posterior circulation strokes can mimic acute vestibular losses, leading to inappropriate treatment. The diagnosis of vestibular neuritis is made based on the clinical manifestation and a bedside otoneurological assessment. In the clinical examination, an evaluation of the vestibulo-ocular reflex is the key element; however, the accuracy of the bedside head impulse test depends on the clinician's experience. Thus, new diagnostic methods are needed to objectify and facilitate such rapid vestibular evaluations. The aim of our paper is to provide a comprehensive review of the video head impulse test's application in the diagnosis of vestibular neuritis. Numerous studies have reported advantages that make this method helpful in detailed otoneurological evaluations; in contrast to the bedside head impulse test, it enables an analysis of all six semicircular canals function and records the covert corrective saccades, which are invisible to the naked eye. As a portable and easy diagnostic tool, it is known to improve the diagnostic accuracy in patients with acute vertigo presenting in the emergency department. Moreover, as it evaluates the vestibulo-ocular reflex across different frequencies, as compared to caloric tests, it can be used as an additional test that is complementary to videonystagmography. Recently, several papers have described the application of the video head impulse test in follow-up and recovery evaluations in patients with vestibular neuritis.

[Investigation of vestibular function in patients with vestibular neuritis]. / Issledovanie vestibulyarnoi funktsii u patsientov s vestibulyarnym neironitom.

Vestibular neuritis occupies the third place in terms of prevalence in the structure of peripheral vestibulopathies, therefore, the choice of optimal diagnostic and differential diagnostic tactics at different stages of the disease is an urgent task. OBJECTIVE: To optimize the diagnostic algorithm for vestibular neuritis based on an assessment of the sensitivity of clinical methods for studying vestibular function in the recovery period of the disease. MATERIAL AND METHODS: A comprehensive assessment of the sensitivity of clinical methods for the study of vestibular function in the acute (up to 14 days: at the time of initial treatment, on the 7th and 14th day) and subacute (up to 3 months: on the 28th and 90th day) periods of the disease in 52 patients with upper vestibular neuritis was carried out. RESULTS: The timing of the processes of restoration of vestibular function after a transferred vestibular neuritis is individual: after 14 days, restoration of vestibular function was recorded in 52% (n=27) patients, after 1 month - in 62% (n=32), after 3 months - in 71% (n=37) patients with upper vestibular neuritis. Statocoordination, statokinetic, oculomotor tests under visual control have the highest sensitivity in the acute period of vestibular neuritis, within up to 7 days from the onset of symptoms. In the subacute period of vestibular neuritis, the study of spontaneous nystagmus and nystagmus in the head shaking test retains high sensitivity only when using special tools (Frenzel goggles or videonystagmography). A decrease in the sensitivity of the head rotation test and the dynamic visual acuity test in the subacute period of vestibular neuritis is associated with the processes of central compensation and the formation of a latent saccade. CONCLUSION: The sensitivity of clinical tests in patients with vestibular neuritis depends on the timing of the examination.

Evolution of Hyperventilation-Induced Nystagmus in Acute Unilateral Vestibulopathy-Interpretative Model and Etiopathogenetic Hypotheses.

Hyperventilation induces metabolic changes that can elicit nystagmus (hyperventilation-induced nystagmus, HVIN) in various vestibular disorders, revealing vestibular imbalance and bringing out central or peripheral asymmetries. In acute unilateral vestibulopathy (AUVP, namely vestibular neuritis), hyperventilation can induce different patterns of nystagmus (excitatory, inhibitory, or negative), disclosing or modifying existing static vestibular asymmetries through its ability to invalidate compensation or increase peripheral excitability. In this context, we followed the evolutionary stages of HVIN in AUVP across 35 consecutive patients, with the goal of assessing alterations in the oculomotor pattern caused by hyperventilation over time. In the acute phase, the incidence of the excitatory pattern (and the strongly excitatory one, consisting of a reversal nystagmus evoked by hyperventilation) was significantly higher compared to the inhibitory pattern; then, a progressive reduction in the incidence of the excitatory pattern and a concomitant gradual increase in the incidence of the inhibitory one were observed in the follow-up period. Assuming the role of the ephaptic effect and the transient loss of vestibular compensation as opposing mechanisms, i.e., excitatory and inhibitory, respectively, the oculomotor pattern evoked by hyperventilation is the result of the interaction of these two factors. The data obtained allowed us to hypothesize an interpretative model regarding the pathogenetic aspects of responses evoked by hyperventilation and the etiologies of the disease: according to our hypotheses, the excitatory pattern implies a neuritic (viral) form of AUVP; instead, the inhibitory (and negative) one can be an expression of both the neuritic (viral) and vascular forms of the disease.

Clinical Significance of Neutrophil-to-Lymphocyte Ratio and Platelet-to-Lymphocyte Ratio in Acute Unilateral Vestibulopathy.

BACKGROUND AND PURPOSE: The neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) have been identified as useful biomarkers for assessing the inflammatory response and for predicting the prognosis of various diseases. This study aimed to determine the clinical significance and effects on prognostic prediction of NLR and PLR in acute unilateral vestibulopathy (AUV). METHODS: We retrospectively recruited 128 patients who were diagnosed with AUV from July 2016 to April 2021, and compared NLR and PLR values between these patients with AUV and age- and sex-matched healthy subjects. We also analyzed the correlations of various clinical parameters with NLR and PLR. RESULTS: NLR and PLR in the AUV group were 3.41±2.80 (mean±standard deviation) and 128.86±67.06, respectively, with only NLR being significantly higher than that in the control group (1.55±0.60, p<0.001). The gain asymmetry of the horizontal vestibulo-ocular reflex (VOR) was slightly larger in patients with high NLR (n=52) than in those with normal NLR (n=76) (41.9%±20.2% vs. 33.6%±17.4%, p=0.048). However, the hospitalization period, preceding infection, canal paresis, and absolute horizontal VOR gain did not differ between patients with high and normal NLR and PLR values. The correlation analyses also revealed that none of the clinical parameters were significantly correlated with NLR or PLR. At 3-month follow-up examinations, NLR and PLR did not differ significantly between patients with and without function recovery of the horizontal VOR. CONCLUSIONS: This study found a high NLR in AUV, suggesting an acute inflammatory status in the vestibular organ. However, the usefulness of NLR and PLR as prognostic markers remains unclear.

Compensatory strategies after an acute unilateral vestibulopathy: a prospective observational study.

PURPOSE: In case of an acute unilateral vestibulopathy (UVP), compensatory strategies such as restoration and adaptation will lead to a decrease in intensity of the symptoms. Although measurements of compensatory strategies are available, currently, an overview taking the different strategies into account is lacking. The objectives of this study are to explore compensatory strategies and to investigate the association between compensatory strategies and patient characteristics. METHODS: Restoration was objectified by the vestibulo-ocular reflex (VOR) gain on the video head impulse test, and adaptation-consisting of visual, multisensory, and behavioral substitution-was objectified by the Visual Vertigo Analog Scale (VVAS), Antwerp Vestibular Compensation Index (AVeCI), and Perez and Rey score (PR score), respectively. Adequate restoration and adaptation levels were interpreted as follows: VOR gain > 0.80, VVAS ≤ 40%, AVeCI > 0 and PR score ≤ 55. RESULTS: Sixty-two UVP patients, 34 men and 28 women, were included with an average age of 52.1 ± 17.3 years. At 10.5 ± 1.4 weeks after onset, 41.9% of the UVP patients reached adequate restoration levels and 58.1-86.9% reached adequate adaptation levels. Furthermore, significant associations were found between (1) restoration status and UVP etiology [Odds Ratio (OR) with 95% CI: 4.167 {1.353;12.828}] and balance performance (OR: 4.400 {1.258;15.386}), (2) visual sensory substitution status and perceived handicap (OR: 8.144 {1.644;40.395}), anxiety (OR: 10.000 {1.579;63.316}) and depression (OR: 16.667 {2.726;101.896}), and (3) behavioral substitution status and balance performance (OR: 4.143 {1.341;12.798}). CONCLUSION: UVP patients with adequate compensatory strategies presented with better balance performance, lower perceived handicap, and lower anxiety and depression scores.

Pharmacological Treatment of Acute Unilateral Vestibulopathy: A Review.

There have been few investigations on the epidemiology, etiology, and medical management of acute unilateral vestibulopathy (AUV). Short-term pharmaceutical resolutions include vestibular symptomatic suppressants, anti-emetics, and some cause-based therapies. Anticholinergics, phenothiazines, antihistamines, antidopaminergics, benzodiazepines, and calcium channel antagonists are examples of vestibular suppressants. Some of these medications may show their effects through multiple mechanisms. In contrast, N-acetyl-L-leucine, Ginkgo biloba, and betahistine improve central vestibular compensation. Currently, AUV pathophysiology is poorly understood. Diverse hypotheses have previously been identified which have brought about some causal treatments presently used. According to some publications, acute administration of anti-inflammatory medications may have a deleterious impact on both post-lesional functional recovery and endogenous adaptive plasticity processes. Thus, some authors do not recommend the use of corticosteroids in AUV. Antivirals are even more contentious in the context of AUV treatment. Although vascular theories have been presented, no verified investigations employing anti-clotting or vasodilator medications have been conducted. There are no standardized treatment protocols for AUV to date, and the pharmacological treatment of AUV is still questionable. This review addresses the most current developments and controversies in AUV medical treatment.

Dose- and application route-dependent effects of betahistine on behavioral recovery and neuroplasticity after acute unilateral labyrinthectomy in rats.

Introduction: Betahistine is widely used for the treatment of various vestibular disorders. However, the approved oral administration route and maximum daily dose are evidently not effective in clinical trials, possibly due to a major first-pass metabolism by monoamine oxidases (MAOs). The current study aimed to test different application routes (i.v./s.c./p.o.), doses, and concurrent medication (with the MAO-B inhibitor selegiline) for their effects on behavioral recovery and cerebral target engagement following unilateral labyrinthectomy (UL) in rats. Methods: Sixty rats were subjected to UL by transtympanic injection of bupivacaine/arsanilic acid and assigned to five treatment groups: i.v. low-dose betahistine (1 mg/kg bid), i.v. high-dose betahistine (10 mg/kg bid), p.o. betahistine (1 mg/kg bid)/selegiline (1 mg/kg once daily), s.c. betahistine (continuous release of 4.8 mg/day), and i.v. normal saline bid (sham treatment; days 1-3 post-UL), respectively. Behavioral testing of postural asymmetry, nystagmus, and mobility in an open field was performed seven times until day 30 post-UL and paralleled by sequential cerebral [18F]-FDG-µPET measurements. Results: The therapeutic effects of betahistine after UL differed in extent and time course and were dependent on the dose, application route, and selegiline co-medication: Postural asymmetry was significantly reduced on 2-3 days post-UL by i.v. high-dose and s.c. betahistine only. No changes were observed in the intensity of nystagmus across groups. When compared to sham treatment, movement distance in the open field increased up to 5-fold from 2 to 30 days post-UL in the s.c., i.v. high-dose, and p.o. betahistine/selegiline groups. [18F]-FDG-µPET showed a dose-dependent rCGM increase in the ipsilesional vestibular nucleus until day 3 post-UL for i.v. high- vs. low-dose betahistine and sham treatment, as well as for p.o. betahistine/selegiline and s.c. betahistine vs. sham treatment. From 1 to 30 days post-UL, rCGM increased in the thalamus bilaterally for i.v. high-dose betahistine, s.c. betahistine, and p.o. betahistine/selegiline vs. saline treatment. Discussion: Betahistine has the potential to augment the recovery of dynamic deficits after UL if the administration protocol is optimized toward higher effective plasma levels. This may be achieved by higher doses, inhibition of MAO-based metabolism, or a parenteral route. In vivo imaging suggests a drug-target engagement in central vestibular networks.

Vestibular rehabilitation improves spontaneous nystagmus normalization in patients with acute unilateral vestibulopathy.

Introduction: Spontaneous nystagmus (SN) can be observed after acute unilateral vestibulopathy (AUVP). The slow phase eye velocity of the SN progressively decreases in darkness as the result of rebalanced neurophysiological activity between both vestibular nuclei, a process that can take several months. Although this compensatory process can occur spontaneously, there is poor evidence that vestibular rehabilitation (VR) can facilitate the process. Methods: We documented the natural time course of SN reduction in patients with AUVP, as well as the effects of VR by means of a unilateral rotation paradigm. In a retrospective study (Study 1: n = 126 AUVP patients), we compared the time course of the SN reduction in patients with VR (n = 33) and without VR (n = 93). In a prospective study (Study 2: n = 42 AUVP patients), we compared the effects of early VR (n = 22; initiated within the first two weeks of symptoms onset) or late VR (n = 20; initiated after the second week of symptoms onset) on the time course of the SN reduction. Results: Study 1 showed shorter median time of SN normalization in patients with VR compared to patients without VR (14 days and 90 days, respectively). Study 2 showed that AUVP patients with early and late VR had a similar median time of SN normalization. The SN slow phase eye velocity was significantly decreased as early as the end of the first VR session in both groups, and kept decreasing at each subsequent VR session. In the early VR group, 38% of the patients had slow phase eye velocity below 2°/s after the first VR session, 100% after the fifth session. Similar findings were observed in the late VR group. Discussion: Taken together, these results indicate that VR with a unidirectional rotation paradigm speeds up the normalization of SN. This effect seems independent of the time between symptoms onset and commencement of VR, but early intervention is recommended to speed up the SN reduction.

Identification of hub genes and pathophysiological mechanism related to acute unilateral vestibulopathy by integrated bioinformatics analysis.

Background: Although many pathological mechanisms and etiological hypotheses of acute unilateral vestibulopathy (AUVP) have been reported, but the actual etiology remains to be elucidated. Objective: This study was based on comprehensive bioinformatics to identify the critical genes of AUVP and explore its pathological mechanism. Methods: Gene expression profiles of AUVP and normal samples were collected from GSE146230 datasets of the Gene Expression Omnibus (GEO) database. Weighted gene co-expression network analysis (WGCNA) was constructed, and the WGCNA R-package extracted significant modules. The limma R-package was applied to identify differentially expressed genes (DEGs). The common genes of practical modules and DEGs were screened for GO and KEGG pathways analysis. The protein-protein interaction (PPI) layout and hub genes validation was created by Cytoscape software using the link from the STRING database. The functions of hub genes were predicted through the CTD (comparative genetics database). Results: A total of 332 common genes were screened from practical modules and DEGs. Functional enrichment analysis revealed that these genes were predominantly associated with inflammation and infection. After construction of PPI, expressions of hub genes, and drawing ROC curves, LILRB2, FPR1, AQP9, and LILRA1 are highly expressed in AUVP (p < 0.05) and have a certain diagnostic efficacy for AUVP (AUC > 0.7), so they were selected as hub genes. The functions of hub genes suggested that the occurrence of AUVP may be related to inflammation, necrosis, hepatomegaly, and other conditions in CTD. Conclusion: LILRB2, FPR1, AQP9, and LILRA1 may play essential roles in developing AUVP, providing new ideas for diagnosing and treating AUVP.

Videooculography "HINTS" in Acute Vestibular Syndrome: A Prospective Study.

Objective: A three-step bedside test ("HINTS": Head Impulse-Nystagmus-Test of Skew), is a well-established way to differentiate peripheral from central causes in patients with acute vestibular syndrome (AVS). Nowadays, the use of videooculography gives physicians the possibility to quantify all eye movements. The goal of this study is to compare the accuracy of VOG "HINTS" (vHINTS) to an expert evaluation. Methods: We performed a prospective study from July 2015 to April 2020 on all patients presenting at the emergency department with signs of AVS. All the patients underwent clinical HINTS (cHINTS) and vHINTS followed by delayed MRI, which served as a gold standard for stroke confirmation. Results: We assessed 46 patients with AVS, 35 patients with acute unilateral vestibulopathy, and 11 patients with stroke. The overall accuracy of vHINTS in detecting a central pathology was 94.2% with 100% sensitivity and 88.9% specificity. Experts, however, assessed cHINTS with a lower accuracy of 88.3%, 90.9% sensitivity, and 85.7% specificity. The agreement between clinical and video head impulse tests was good, whereas for nystagmus direction was fair. Conclusions: vHINTS proved to be very accurate in detecting strokes in patients AVS, with 9% points better sensitivity than the expert. The evaluation of nystagmus direction was the most difficult part of HINTS.

Acute unilateral vestibulopathy/vestibular neuritis: Diagnostic criteria.

This paper describes the diagnostic criteria for Acute Unilateral Vestibulopathy (AUVP), a synonym for vestibular neuritis, as defined by the Committee for the Classification of Vestibular Disorders of the Bárány Society. AUVP manifests as an acute vestibular syndrome due to an acute unilateral loss of peripheral vestibular function without evidence for acute central or acute audiological symptoms or signs. This implies that the diagnosis of AUVP is based on the patient history, bedside examination, and, if necessary, laboratory evaluation. The leading symptom is an acute or rarely subacute onset of spinning or non-spinning vertigo with unsteadiness, nausea/vomiting and/or oscillopsia. A leading clinical sign is a spontaneous peripheral vestibular nystagmus, which is direction-fixed and enhanced by removal of visual fixation with a trajectory appropriate to the semicircular canal afferents involved (generally horizontal-torsional). The diagnostic criteria were classified by the committee for four categories: 1. "Acute Unilateral Vestibulopathy", 2. "Acute Unilateral Vestibulopathy in Evolution", 3. "Probable Acute Unilateral Vestibulopathy" and 4. "History of Acute Unilateral Vestibulopathy". The specific diagnostic criteria for these are as follows:"Acute Unilateral Vestibulopathy": A) Acute or subacute onset of sustained spinning or non-spinning vertigo (i.e., an acute vestibular syndrome) of moderate to severe intensity with symptoms lasting for at least 24 hours. B) Spontaneous peripheral vestibular nystagmus with a trajectory appropriate to the semicircular canal afferents involved, generally horizontal-torsional, direction-fixed, and enhanced by removal of visual fixation. C) Unambiguous evidence of reduced VOR function on the side opposite the direction of the fast phase of the spontaneous nystagmus. D) No evidence for acute central neurological, otological or audiological symptoms. E) No acute central neurological signs, namely no central ocular motor or central vestibular signs, in particular no pronounced skew deviation, no gaze-evoked nystagmus, and no acute audiologic or otological signs. F) Not better accounted for by another disease or disorder."Acute Unilateral Vestibulopathy in Evolution": A) Acute or subacute onset of sustained spinning or non-spinning vertigo with continuous symptoms for more than 3 hours, but not yet lasting for at least 24 h hours, when patient is seen; B) - F) as above. This category is useful for diagnostic reasons to differentiate from acute central vestibular syndromes, to initiate specific treatments, and for research to include patients in clinical studies."Probable Acute Unilateral Vestibulopathy": Identical to AUVP except that the unilateral VOR deficit is not clearly observed or documented."History of acute unilateral vestibulopathy": A) History of acute or subacute onset of vertigo lasting at least 24 hours and slowly decreasing in intensity. B) No history of simultaneous acute audiological or central neurological symptoms. C) Unambiguous evidence of unilaterally reduced VOR function. D) No history of simultaneous acute central neurological signs, namely no central ocular motor or central vestibular signs and no acute audiological or otological signs. E) Not better accounted for by another disease or disorder. This category allows a diagnosis in patients presenting with a unilateral peripheral vestibular deficit and a history of an acute vestibular syndrome who are examined well after the acute phase.It is important to note that there is no definite test for AUVP. Therefore, its diagnosis requires the exclusion of central lesions as well as a variety of other peripheral vestibular disorders. Finally, this consensus paper will discuss other aspects of AUVP such as etiology, pathophysiology and laboratory examinations if they are directly relevant to the classification criteria.

Can hyperventilation test and duration of spontaneous nystagmus help differentiate between vascular and inflammatory aetiology of acute unilateral vestibular deficit?

Objective: To relate clinically the duration of spontaneous nystagmus and hyperventilation-induced nystagmus (HVIN) to vascular or inflammatory aetiology of acute unilateral vestibulopathy observed in a very early stage. Methods: This is a retrospective study on 198 patients with acute unilateral vestibulopathy. Results: In the short-lasting nystagmus group (spontaneous nystagmus < 48 h), mean age and cardiovascular risk were significantly higher; the rates of negative HVIN and paretic HVIN were 41.7% and 58.3%, respectively. In the long-lasting nystagmus group (spontaneous nystagmus > 48 h), mean age and vascular risk were lower; HVIN was absent in 12.6% of the cases, HVIN excitatory patterns were observed in 40.3% of cases and a paretic pattern in 47.1%. Conclusions: A vascular aetiology should be considered the most likely in patients with spontaneous nystagmus < 48 hours: all patients were > 60 years old, cardiovascular risk was higher and HVIN was always absent or paretic. In the group with nystagmus > 48 hours, similarly, data indicate a higher incidence of paretic HVIN in older patients and higher vascular risk, even if the data does not allow us to lean clearly towards one of the two aetiological hypotheses.

Acute vestibular syndrome: is skew deviation a central sign?

OBJECTIVE: Skew deviation results from a dysfunction of the graviceptive pathways in patients with an acute vestibular syndrome (AVS) leading to vertical diplopia due to vertical ocular misalignment. It is considered as a central sign, however, the prevalence of skew and the accuracy of its test is not well known . METHODS: We performed a prospective study from February 2015 until September 2020 of all patients presenting at our emergency department (ED) with signs of AVS. All patients underwent clinical HINTS and video test of skew (vTS) followed by a delayed MRI, which served as a gold standard for vestibular stroke confirmation. RESULTS: We assessed 58 healthy subjects, 53 acute unilateral vestibulopathy patients (AUVP) and 24 stroke patients. Skew deviation prevalence was 24% in AUVP and 29% in strokes. For a positive clinical test of skew, the cut-off of vertical misalignment was 3 deg with a very low sensitivity of 15% and specificity of 98.2%. The sensitivity of vTS was 29.2% with a specificity of 75.5%. CONCLUSIONS: Contrary to prior knowledge, skew deviation proved to be more prevalent in patients with AVS and occurred in every forth patient with AUVP. Large skew deviations (> 3.3 deg), were pointing toward a central lesion. Clinical and video test of skew offered little additional diagnostic value compared to other diagnostic tests such as the head impulse test and nystagmus test. Video test of skew could aid to quantify skew in the ED setting in which neurotological expertise is not always readily available.

The Role of the Functional Head Impulse Test with and without Optokinetic Stimuli in Vestibular Migraine and Acute Unilateral Vestibulopathy: Discovering a Dynamic Visual Dependence.

(1) Background: Visually induced vertigo (i.e., vertigo provoked by moving visual scenes) can be considered a noticeable feature of vestibular migraines (VM) and can be present in patients suffering from acute unilateral vestibulopathy (AUV). Hypersensitivity to moving or conflicting visual stimulation is named visual dependence. (2) Methods: Visuo-vestibular interactions were analyzed via the functional Head Impulse Test (fHIT) with and without optokinetic stimulation (o-fHIT) in 25 patients with VM, in 20 subjects affected by AUV, and in 20 healthy subjects. We calculated the percentage of correct answers (%CA) without and with the addition of the optokinetic background (OB). (3) In VM groups, the %CA on the fHIT was 92.07% without OB and 73.66% with OB. A significant difference was found between %CA on the deficit side and that on the normal side in AUV, both without OB and with OB. (4) Conclusions: The fHIT results in terms of %CA with and without OB could be useful to identify the presence of a dynamic visual dependence, especially in patients suffering from VM. The difference in %CA with and without OB could provide instrumental support to help correctly identify subjects suffering from VM. We propose the use of the fHIT in clinical practice whenever there is a need to highlight a condition of dynamic visual dependence.

Prognosis after acute unilateral vestibulopathy: Usefulness of the suppression head impulse paradigm (SHIMP).

OBJECTIVES: This cross-sectional study aims to describe the features of the suppression head impulse paradigm (SHIMP) in acute unilateral vestibulopathy (AUV) and to define its role in predicting the recovery of patients. METHODS: Thirty patients diagnosed with AUV were retrospectively analyzed. The dizziness handicap inventory score and video head impulse test parameters performed 4-8 weeks from the AUV onset constituted the main outcome measures. Patients with a worse recovery (Group 1) and patients who recovered spontaneously (Group 2) were compared. RESULTS: The SHIMP vestibulo-ocular reflex (VOR) gain was statistically significantly lower than the conventional head impulse paradigm (HIMP) VOR gain (P < 0.001). The SHIMP VOR gain was negatively correlated with the DHI (P < 0.001) and was positively correlated with the HIMP VOR gain (P < 0.001) and the SHIMP overt saccades (%) (P < 0.001). Patients with a worse recovery exhibited the following: higher DHI (P < 0.001), lower SHIMP and HIMP VOR gain (P < 0.001 and P = 0.007, respectively), and lower SHIMP and greater HIMP overt saccade prevalence values (P = 0.007 and P = 0.032, respectively). CONCLUSIONS: The SHIMP and HIMP help in improving our approach to AUV. SHIMP appears to better identify the extent of the vestibular damage in patient suffering from AUV than HIMP and could provide interesting information about the course of the disease. Particularly, the analysis of SHIMP VOR gain and overt saccade prevalence would provide useful information about the recovery of patients.