Cellular Processes Induced by HSV-1 Infections in Vestibular Neuritis.

Herpesvirus is a prevalent pathogen that primarily infects human epithelial cells and has the ability to reside in neurons. In the field of otolaryngology, herpesvirus infection primarily leads to hearing loss and vestibular neuritis and is considered the primary hypothesis regarding the pathogenesis of vestibular neuritis. In this review, we provide a summary of the effects of the herpes virus on cellular processes in both host cells and immune cells, with a focus on HSV-1 as illustrative examples.

Is Inadequate Water Intake a Risk Factor for Vestibular Disorders?

BACKGROUND: Water is a vital nutrient for the human body system and failing to consume enough water could cause health problems. The purpose of this study is to investigate the relationship between water intake and vestibular system disorders. METHODS: Data from 93 patients (aged between 20 and 76 years) with vestibular disorders were analyzed in the study. The mean age of the patients was 46.96 ±13.94 years (female: 45.68 ±13.45, male: 49.96 ±14.85), and 69.9% (n=65) were female. Participants were sub-categorized into diagnostic groups as follows: benign paroxysmal positional vertigo, Meniere's disease, vestibular neuritis, vestibular migraine, and persistent postural perceptual dizziness. The water intake information was analyzed for total water, plain water, and caffeinated beverages separately and compared between groups. RESULTS: There was a significant difference between vestibular neuritis and benign paroxysmal positional vertigo (P < .001) and also between vestibular neuritis and Meniere's disease (P = .021) in terms of the intake values of plain water and total water. No significant difference was found between groups in caffeinated beverages intake (P = .151), and it was found that there is no statistically significant difference in plain water and total water intake in terms of gender (P > .05). CONCLUSION: The most significant result of this study is that inadequate water intake can be a risk factor for some forms of peripheral vestibular disorders. People should be informed about the importance of drinking water and be encouraged to increase their water intake.

Isolated cerebellar nodulus infarction: Two case reports and literature review.

BACKGROUND: Isolated cerebellar nodulus infarction (ICNI) is rare and has great clinical similarity with acute peripheral vestibulopathy (APV), from which it is difficult to distinguish. We report two cases of ICNI followed by a literature review to identify the discriminant clinical elements that differentiate ICNI from APV. METHODS: We describe in detail our 2 cases. Besides, a literature search in Medline via PubMed and Scopus was performed up to May 17, 2020. Clinical characteristics, mainly of well-described cases, were extracted and analyzed. RESULTS: Our search yielded 43 total publications, among which 13 were selected, including 23 patients. Spontaneous or positional rotatory vertigo with unidirectional spontaneous horizontal nystagmus, associated with the postural imbalance and unilateral lateropulsion or fall on Romberg's test, was the most common clinical picture. According to our literature review, the discriminant clinical elements which differentiate ICNI from APV were direction-changing gaze-evoked nystagmus, bilateral lateropulsion or fall on Romberg's test, and normal horizontal head impulse test. Our two patients reported a positional fleeting abnormal visual perception of spatial orientation of objects. We proposed this symptom as a discriminant clinical element. CONCLUSION: The ICNI constitutes a difficult differential diagnosis of APV. Through our two patients reported here, we proposed a supplementary discriminant symptom helpful for the clinical diagnosis.

A case series of vestibular symptoms in positive or suspected COVID-19 patients.

Respiratory symptoms are the most common presentation of an acute COVID-19 infection, but thromboembolic phenomena, encephalopathy and other neurological symptoms have been reported. With these case series, we present multiple presentations of COVID-19 induced vestibular symptoms namely dizziness, vertigo and nystagmus. The patients reported in this case series are from different parts of the world, belong to different age groups and had manifested these symptoms in different periods of the pandemic. The pathophysiology of vestibular neuritis induced by COVID-19 is similar to any other viral infection. Whether in the inpatient or outpatient settings, COVID-19 should be considered in the differential diagnosis for patients presenting with these symptoms, irrespective of the presence of respiratory symptoms or hypoxia.

Acute vestibular syndrome and hearing loss mimicking labyrinthitis as initial presentation of multiple sclerosis.

Acute vestibular syndrome is most often caused by vestibular neuritis or stroke, although demyelinating diseases may be responsible for 4% of all AVS episodes. The authors present the case of a previously healthy 17-year-old female patient complaining of spontaneous vertigo and right-sided hearing loss. Otoneurological examination suggested a peripheral vestibular cause and video head impulse test revealed a reduced vestibulo-ocular reflex gain. The presence of sensorineural hearing loss raised the suspicion of a central cause and prompted imaging evaluation. A brain MRI evidenced demyelinating lesions in the right middle cerebellar peduncle and the patient was ultimately diagnosed with Multiple Sclerosis.

Can Hashimoto's thyroiditis cause vertigo? [Czy choroba Hashimoto moze byc przyczyna zawrotów glowy?].

Vertigo and balance disorders are common symptoms reported by approximately 15-20% of the adult population worldwide. For many years thyroid diseases have been suspected as the cause of vertigo by ENT physicians. Almost every patient hospitalised due to severe vertigo is investigated for thyroid disease as a suspected cause of acute vestibulopathy. The issue presented in this paper is related to a difficult and poorly understood relationship between autoimmune thyroid disease and peripheral vertigo.

[A role of vascular risk factors in the development of peripheral vestibulopathy]. / Rol' faktorov serdechno-sosudistogo riska v razvitii perifericheskikh vestibulopatii.

The development of peripheral vestibular disorders are often thought to be associated with vascular mechanisms, taking into account terminal type of inner ear blood supply and other predisposing factors. A number of studies indicates a high frequency of vascular risk factors in the patients with vestibular neuronitis and benign paroxysmal positional vertigo (BPPV). According to other results, migraine is widely spread among patients with Meniere's disease and BPPV. However currently there is no evidence for casual relationship between vascular factors and development of peripheral vestibulopathy. The only exclusion is labyrinthine infarction, which develops as a result of posterior circulation disorder. More research is needed in this area.

[Isolated vertigo as the first symptom of posterior circulation infarction:reporot of 11 cases].

Objective:To analyze the clinical characteristics of patients with cerebellar and brainstem infarction who initially presented with isolated vertigo to avoid misdiagnosing of this disease.Method:Eleven patients with cerebellar and brainstem infarction who initially presented with isolated vertigo treated in our clinic between January 2014 and September 2017 were reviewed and the clinical characteristics and imaging presentation of the patients were evaluated.Result:Vertigo as the first attack was in 5 cases, recurrent attacks was in 6 cases,10 cases were with vascular risk factors except for 1 case, initially diagnosed as vestibular neuritis was 4 cases, Meniere's disease was 1 case, posterior circulartion ischemia was 1 case,and unknown causes was 5 cases; delayed neurological symptoms and signs occurring was 4 cases, but not in other cases; finally determined by brain MRI as acute cerebellar infarction was 5 cases, brainstem infarction was 5 cases, and concurrent cerebellar and brainstem infarction was 1 case. All patients had good prognosis.Conclusion:Isolated vertigo due to posterior circulation infarction is easy to be misdiagnosed as peripheral vertigo.Patients presenting with isolated vertigo, when with vascular risk factors, should receive MRI and DWI examinations. Properly diagnosis and treatment may lead a good prognosis.

Management of Recurrent Vestibular Neuritis in a Patient Treated for Rheumatoid Arthritis.

PURPOSE: This clinical report is presented to describe how results of vestibular function testing were considered along with other medical history to develop a management plan that was ultimately successful. METHOD: The patient underwent audio-vestibular assessment including comprehensive audiogram, videonystagmography, cervical vestibular evoked myogenic potential, and postural stability testing. RESULTS: Results from initial testing were most consistent with uncompensated peripheral vestibular dysfunction affecting the right superior vestibular nerve. These results, considered along with history and symptoms, supported vestibular neuritis. After a second vertigo event, we became concerned about the potential temporal association between the patient's rheumatoid arthritis treatment and symptom onset. It is established that treatment for rheumatoid arthritis can exacerbate latent viral issues, but this has not specifically been reported for vestibular neuritis. There are reports in the literature in which patients successfully used viral suppressant medication to decrease viral activity while they were able to continue benefiting from immunosuppressive therapy. We hypothesized that, if the current patient's vestibular neuritis events were related to her treatment for rheumatoid arthritis, she may also benefit from use of viral suppressant medication while continuing her otherwise successful immunosuppressive intervention. CONCLUSIONS: Patients treated with biologic disease-modifying antirheumatic drugs are more susceptible to viral issues, and this may include vestibular neuritis. For the current case, identifying this possibility and recommending viral suppressant medication allowed her to continue with successful treatment of rheumatoid arthritis while avoiding additional vertigo events.

Vertigo in Vestibular Schwannoma Patients Due to Other Pathologies.

OBJECTIVE: To report findings from a cohort of vestibular schwannoma (VS) patients presenting with vertigo from a secondary comorbid vestibular disorder; and to discuss management strategies for this subset of patients presenting with both episodic vertigo and VS. PATIENTS: All VS patients who presented with vertigo as the primary symptom from 2012 to 2015 and endorsing no other major complaints were examined. INTERVENTION: Treatment with migraine lifestyle and prophylactic therapy, or Epley maneuver. MAIN OUTCOME MEASURE: Resolution of vertigo following medical treatment alone. RESULTS: Of the nine patients studied, seven (78%) suffered from vestibular migraine, and two (22%) experienced benign positional vertigo. All patients experienced complete resolution of symptoms after treatment. As a result of symptomatic improvement, seven patients (78%) avoided surgery in favor of observation, while two patients (22%) underwent radiosurgery due to continued tumor growth and other nonvertigo symptoms. CONCLUSION: VS patients can sometimes present with a history of recurrent episodic vertigo. The etiology of the vertigo could be due to the tumor itself or may be due to an underlying comorbidity such as vestibular migraine or benign positional vertigo. VS patients presenting with vertigo should undergo a standard vertigo history and examination to identify other potential causes of vertigo. Most VS patients in our cohort avoided intervention and had resolution of their vertigo.

[Idiopathic cranial nerve failure]. / Idiopathische Hirnnervenausfälle.

Cranial nerve lesions require a thorough diagnostic work-up and known etiologies have to be excluded before the term idiopathic can be considered. The focus of the present review is on idiopathic peripheral facial nerve paralysis (Bell's palsy) for which this terminology has been established. For all other cranial nerve lesions the typical clinical signs, established etiologies and possible diagnostic pitfalls are discussed.

Acute unilateral peripheral vestibulopathy in neurosyphilis.

INTRODUCTION: Neurosyphilis producing basal meningitis presenting as sequential transient cranial nerve palsies was well recognized before the antibiotic era. OBJECTIVE: To report two patients presenting with acute unilateral peripheral vestibulopathy due to syphilitic basal meningitis. RESULTS: In Case 1 basal meningitis occurred early in the secondary phase of the infection, in Case 2 in the late latent phase. The diagnosis was not made immediately in either case; in Case 1 after previous presentation with increasing hearing loss and then with facial palsy and then a subsequent presentation with optic neuritis; in Case 2 after investigation for possible lymphoma. CONCLUSION: Syphilitic basal meningitis in either the secondary or in the latent phase can present as acute unilateral peripheral vestibulopathy with transient involvement of the facial or auditory nerve.

Diagnosis and Treatment of Vestibular Neuritis/Neuronitis or Peripheral Vestibulopathy (PVP)? Open Questions and Possible Answers.

: The acute vestibular syndrome is a clinically defined entity consisting of vertigo or dizziness that develops acutely over minutes to hours and is accompanied by nausea/vomiting, gait instability, head motion intolerance, and nystagmus, while persisting over a day or more. When it is caused by a peripheral vestibular lesion and is not associated with clinically manifest auditory deficits, it is mostly labeled vestibular neuritis/neuronitis/neuropathy or sometimes peripheral vestibulopathy. Here, we propose hypotheses and discuss current research advances on viral or vascular factors in the pathogenesis, the recurrence, the site of lesion, old and new treatment options, contraindicated measures, the differential diagnosis, and the prognosis of vestibular neuritis/neuronitis/neuropathy or vestibulopathy. Possibly, other structures than the vestibular nerve are also involved in the pathogenetic process and the label peripheral vestibulopathy would be more apt.

A connection between neurovascular conflicts within the cerebellopontine angle and vestibular neuritis, a case controlled cohort study.

This retrospective, observer blinded case-control study aims to compare the prevalence of neurovascular conflicts (NVCs) of the vestibulocochlear nerve and the anterior inferior cerebellar artery (AICA) in patients presenting with clinical signs of acute vestibular neuritis with and without subsequent objective vestibular function loss (VFL). 58 acute cases of clinically suspected acute vestibular neuritis were investigated with same day cranial MRI at a tertiary referral centre and compared to 61 asymptomatic controls. The prevalence of NVCs in cases with objective VFL were also compared to cases without VFL. Radiologists described the NVC as "no contact" (Grade 0), "contact < 2 mm" (Grade 1), "contact > 2 mm" (Grade 2) and "vascular loop presence" (Grade 3) without knowledge of neurotological data. Neurotological data was collected without knowledge of MRI findings. Vestibular function was tested by bithermic caloric irrigation. 26 cases (45%) showed caloric VFL (Group A), whereas 32 (55%) exhibited no VFL (Group B). Group A included 13 cases with NVCs (50%), Group B included 26 NVC cases (82%) (p = 0.012) and the control group included 16 individuals (26%) (p < 0.001 for comparison of all 3 groups). Group B had a significantly higher NVC-Grading than Group A (p = 0.009). There was no statistically significant association between NVCs and either SNHL or tinnitus (p > 0.05). Our results suggest that patients presenting with clinical signs of acute vestibular neuritis who show symmetrical caloric vestibular function test results have a significantly higher NVC prevalence in the cerebellopontine angle.

Isolated Vestibular Suppression Impairment With Vestibular Migraine: A Phenotypic CANVAS Variant.

HYPOTHESIS: Cerebellar Ataxia with Neuropathy and Vestibular Areflexia (CANVAS) is likely to have a genetic basis. We describe the unique eye movement features of a possible phenotypic CANVAS variant. BACKGROUND: The patient comes from a large CANVAS kindred (four out of nine siblings) and has sensory neuropathy, cerebellar eye signs, and vestibular migraine (VM), but otherwise normal vestibular function. METHODS: We recorded eye and head movements using the gold standard scleral search coil technique: in the patient, a close relative with mild sensory neuropathy, and a normal control. RESULTS: At ≥ 0.8 Hz vestibulo-ocular reflex suppression (VORS) was significantly smaller in the patient. At 1 Hz, the patient's VORS was almost two times worse than the control, and five times worse at 1.6 Hz. The patient's VORS deficiency was observed with the naked eye as an inability to keep the eye stationary during imposed sinusoidal head rotation at ∼ 1 Hz. At ≤ 0.8 Hz the patient had 10 to 20% lower smooth pursuit function compared with both the patient-relative and control subjects. This difference was difficult to detect by the naked eye. Saccadic oculomotor and vestibular function was normal. CONCLUSION: We propose that impaired VORS and VM are because of similar, but distinct, consequences of selective partial cerebellar dysfunction. The patient's VORS data are consistent with a CANVAS neuropathological study showing selective degeneration of the dorsal vermis of the cerebellum, a region thought to be important for VORS. Taken together our findings suggest the patient is a CANVAS variant. We hypothesise VORS impairment is part of CANVAS, but not revealed because of vestibular loss.

Vertigo with a Vestibular Dysfunction in Children During Respiratory Tract Infections.

Sudden balance disorders with violent vegetative symptoms (nausea and vomiting) pose a diagnostic and therapeutic problem. In children vertigo/dizziness with symptoms of vestibular dysfunction is rare, but as vascular etiology is unlikely in children such symptoms arouse concern. This article presents two cases of this type of vertigo. The patients were two boys (6 and 9 years old). They came down with similar symptoms: sudden dizziness, disabled walking, nausea and vomiting, spontaneous nystagmus, and a positive Romberg test. The onset of the balance disorder was preceded by respiratory infection: common cold with symptoms of inflammation of the mucous membrane in the nose and throat. Laboratory tests revealed increased levels of C-reactive protein only in the older boy. Neuroinfection and a displacement process were ruled out. Videonystagmography revealed vestibular dysfunction and vestibular neuronitis on the left side.

Superior Versus Inferior Vestibular Neuritis: Are There Intrinsic Differences in Infection, Reactivation, or Production of Infectious Particles Between the Vestibular Ganglia?

HYPOTHESIS: Intrinsic differences in neurons of the vestibular ganglia result in the increased likelihood of superior vestibular ganglion involvement in vestibular neuritis. BACKGROUND: Vestibular neuritis is hypothesized to result from herpes simplex type I (HSV1) infection or reactivation in vestibular ganglia. Involvement of the inferior vestibular ganglion is extremely rare in patients with vestibular neuritis. METHODS: Primary cultures of rat superior and inferior vestibular ganglion neurons (VGNs) were cultivated separately. Neurons were lytically and latently infected with HSV1 with a US11-green fluorescent protein (GFP) chimera. Percentage lytic infection and baseline reactivation was assessed by microscopy for GFP fluorescence. Trichostatin-A (TSA) was used to stimulate HSV1 reactivation. Virion production was assessed by viral titers. Relative numbers of latency-associated (LAT) transcripts were determined by real-time reverse-transcription polymerase chain reaction (real-time RT-PCR). RESULTS: Lytic infection rates were equivalent between the two ganglia (p > 0.05). Lytic infections yielded similar amounts of plaque-forming units (p > 0.05). Relative amounts of LAT transcripts did not differ between latently infected superior and inferior VGNs. Latently infected cultures showed no differences in rates of baseline and TSA-induced HSV1 reactivation (p > 0.05). Production of virions was not significantly different between reactivated, latently infected superior versus inferior VGNs (p = 0.45). CONCLUSION: Differences in prevalence of superior and inferior vestibular neuritis do not result from intrinsic differences in HSV1 infection or virion production of these neurons. Other factors, such as the length and width of the bony canal containing the ganglia and nerves, account for the greater involvement of the superior vestibular ganglion in vestibular neuritis.

Electrophysiologic vestibular evaluation in type 2 diabetic and prediabetic patients: Air conduction ocular and cervical vestibular evoked myogenic potentials.

OBJECTIVE: Chronically increased blood glucose levels may affect the vestibular system by damaging cells and neural structures in diabetes mellitus (DM). We aimed to search the effects of neurovascular degeneration on the vestibular system in type 2 DM and prediabetic patients by using air-conducted ocular (oVEMP) and cervical (cVEMP) vestibular evoked myogenic potentials. DESIGN: Prospective study. STUDY SAMPLE: Thirty diabetic, 30 prediabetic patients, and 31 age- and sex-matched controls having no peripheral or central vestibular disease, were enrolled. All participants were evaluated by audiovestibular tests, oVEMP, and cVEMP. RESULTS: In the diabetic group, mean values of both oVEMP and cVEMP p1, n1 latencies were significantly longer compared to the prediabetic group and the control group, whereas latencies were similar in prediabetic and the control groups. Bilateral neural dysfunction was recognized in both tests and lateralization was not seen in VEMP asymmetric ratios. In the diabetic group, prevalence of pathological p1 and n1 latencies in oVEMP were 30.4% and 37.5%, whereas they were 53.7%, 59.3% in cVEMP, respectively. p1 latencies of cVEMP and oVEMP were positively correlated with HbA1c and fasting plasma glucose level in the diabetic group. CONCLUSION: Subclinical vestibular neuropathy can be a newly defined diabetes-related complication.

Is vestibular neuritis an immune related vestibular neuropathy inducing vertigo?

OBJECTIVES: To review the current knowledge of the aetiology of vestibular neuritis including viral infections, vascular occlusion, and immunomediated mechanisms and to discuss the pathogenesis with relevance to pharmacotherapy. SYSTEMATIC REVIEW METHODOLOGY: Relevant publications on the aetiology and treatment of vestibular neuritis from 1909 to 2013 were analysed. RESULTS AND CONCLUSIONS: Vestibular neuritis is the second most common cause of peripheral vestibular vertigo and is due to a sudden unilateral loss of vestibular function. Vestibular neuronitis is a disorder thought to represent the vestibular-nerve equivalent of sudden sensorineural hearing loss. Histopathological studies of patients who died from unrelated clinical problems have demonstrated degeneration of the superior vestibular nerve. The characteristic signs and symptoms include sudden and prolonged vertigo, the absence of auditory symptoms, and the absence of other neurological symptoms. The aetiology and pathogenesis of the condition remain unknown. Proposed theories of causation include viral infections, vascular occlusion, and immunomediated mechanisms. The management of vestibular neuritis involves symptomatic treatment with antivertiginous drugs, causal treatment with corticosteroids, and physical therapy. Antiviral agents did not improve the outcomes.