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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.

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.

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., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

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.

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.

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.

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., Competing Interests: The authors of this article and the planning committee members and staff have no relevant financial relationships with commercial interests to disclose., (Copyright© by the Editorial Department of Journal of Clinical Otorhinolaryngology Head and Neck Surgery.)

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.

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.

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.

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., (Copyright © 2017 Elsevier B.V. All rights reserved.)

: 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.

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., (© Copyright by Società Italiana di Otorinolaringologia e Chirurgia Cervico-Facciale, Rome, Italy.)

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.

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.

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.

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.

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.

Vestibular neuritis is a sudden unilateral peripheral vestibular deficit of unknown origin without associated hearing loss. It is the second cause of peripheral vertigo after Benign Paroxysmal Positional Vertigo (BPPV). The etiology remains unclear and some treatments are still controversial. The prognosis is good. The differential diagnosis of the disease mainly includes an acute vertigo of central origin. This article summarizes the management and prognosis of vestibular neuritis.

Vestibular neuritis is the most common cause of acute spontaneous vertigo. Vestibular neuritis is ascribed to acute unilateral loss of vestibular function, probably due to reactivation of herpes simplex virus in the vestibular ganglia. The diagnostic hallmarks of vestibular neuritis are spontaneous horizontal-torsional nystagmus beating away from the lesion side, abnormal head impulse test for the involved semicircular canals, ipsilesional caloric paresis, decreased responses of vestibular-evoked myogenic potentials during stimulation of the affected ear, and unsteadiness with a falling tendency toward the lesion side. Vestibular neuritis preferentially involves the superior vestibular labyrinth and its afferents. Accordingly, the function of the posterior semicircular canal and saccule, which constitute the inferior vestibular labyrinth, is mostly spared in vestibular neuritis. However, because the rare subtype of inferior vestibular neuritis lacks the typical features of vestibular neuritis, it may be misdiagnosed as a central vestibular disorder. Even in the patient with the typical pattern of spontaneous nystagmus observed in vestibular neuritis, brain imaging is indicated when the patient has unprecedented headache, negative head impulse test, severe unsteadiness, or no recovery within 1 to 2 days. Symptomatic medication is indicated only during the acute phase to relieve the vertigo and nausea/vomiting. Vestibular rehabilitation hastens the recovery. The efficacy of topical and systemic steroids requires further validation., (Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.)

Conclusion: It is suggested that vertigo in patients with Ramsay Hunt syndrome is mostly induced by superior vestibular neuritis consecutive to the reactivation of varicella-zoster virus (VZV) infection from the geniculate ganglion through the faciovestibular anastomosis. Refractory hearing loss in patients with Ramsay Hunt syndrome may be due to cochlear neuritis following the spread of VZV., Objectives: An attempt was made to selectively identify vestibulocochlear nerves in the internal auditory canal (IAC) on gadolinium (Gd)-enhanced MRI in patients with Ramsay Hunt syndrome., Methods: Fourteen patients with Ramsay Hunt syndrome presenting with facial palsy, herpes zoster oticus, vertigo, and/or sensorineural hearing loss were scanned on 1.5 T MRI enhanced with Gd. Perpendicular section images of the IAC were reconstructed to identify the facial, superior, and inferior vestibular nerves and the cochlear nerves separately., Results: All except one of the patients with Ramsay Hunt syndrome with vertigo showed both canal paresis on the caloric test and Gd enhancement of the superior vestibular nerve in the IAC on MRI. Among 10 patients with hearing loss, 3 patients with severe to moderate sensorineural hearing loss showed Gd enhancement of the cochlear nerve in the IAC on MRI.

The recurrent nature of the 3 most common vestibulopathies suggests a recurrent cause. Histopathology in temporal bones from patients with these syndromes - vestibular neuronitis (VN, n = 7), Ménière's disease (MD, n = 8) and benign paroxysmal positional vertigo (BPPV, n = 5) - shows focal degeneration of vestibular nerve axons and degenerated nearby facial nerve meatal ganglion cells. Transmission electron microscopic confirmation of intracytoplasmic viral particles in surgically excised vestibular nerves from patients with VN and MD support a viral etiology in these vestibulopathies. Antiviral treatment of these syndromes in a series of 211 patients with a 3- to 8-year follow-up resulted in complete control of vertigo in VN (88%), MD (90%) and BPPV (60%)., (Copyright © 2013 S. Karger AG, Basel.)

Purpose of Review: The field of neuro-otology has advanced substantially over the past 150 years. The function of the vestibular system was presumed to be audiologic prior to the groundbreaking work of Prosper Ménière in the late 1800s. Since that time, scientific discovery has advanced our knowledge of the physiology and the pathophysiology of the vestibular system. This article describes where we have been, where we are now, and where we need to go from here., Recent Findings: Some of the important recent advances include: (1) improved imaging of the brain and inner ear, (2) development of new eye movement recording and analysis techniques, (3) development of new tests of otolith function, (4) particle repositioning maneuvers for all types of benign paroxysmal positional vertigo, and (5) improved bedside diagnosis and treatment of vestibular neuritis., Summary: The cause and treatment for some common neuro-otologic disorders is now well delineated. The diagnosis and management of less common disorders has improved as well. Future work is still required to advance the science of vestibular physiology and pathophysiology and ultimately to discover new ways to improve the health of patients with these disorders.

To avoid serious causes of dizziness and establishing preliminary diagnosis is usually enough sighting history taking and physical examination of the patient. Great importance is self-presenting patients with complaints of dizziness. In recent years, for treatment of various types vestybulopatiy, but also for the prevention of attacks, successfully used betahistyn hydrochloride, which improves the quality of care and well-being of the patient.

Vertigo is a fairly common complaint encountered by medics. It is very upsetting and unpleasant for the patient, but it is usually benign and resolves on its own. However, it is vital that the medic be able to differentiate between common vertigo and a more serious condition like stroke. Careful attention to history and physical exam will allow medics to make the right determinations.

Conclusion: Our herpes simplex virus (HSV) labyrinthitis mouse model suggests that HSV infection induces vestibular neuritis and sudden deafness., Objective: Viral labyrinthitis has been postulated to play a role in vestibular neuritis and sudden deafness. We established a mouse model to investigate the pathogenesis of HSV-induced labyrinthitis. The relationship between HSV infection and apoptosis in the labyrinth was assessed., Methods: HSV types 1 and 2 were inoculated into the middle ear of mice, and the function of the cochlear and vestibular nerves was assessed. Histopathological changes were examined with hematoxylin and eosin staining. Anti-HSV immunohistochemistry staining and TUNEL staining were done to investigate the relationship between HSV-infected cells and apoptotic cells., Results: Hearing loss and vestibular dysfunction were observed in all mice after inoculation of HSV type 1 or 2. In the cochlear duct, columnar epithelial cells in the stria vascularis were infected with HSV, but only a portion of the infected cells underwent apoptosis. In contrast, many uninfected cells in the spiral organ of Corti were apoptotic. Vestibular dysfunction was observed when vestibular ganglion cells were largely infected, but not apoptotic. These findings recapitulate sudden deafness and vestibular neuritis described in patients.

The epidemiology, diagnostic features, differential diagnosis, and treatment of vestibular neuritis are reviewed. The authors present considerations for physical examination, imaging, and management in both the acute and chronic phases of this disease. The authors also present a dizziness questionnaire in the Appendix of this publication., (Copyright © 2011 Elsevier Inc. All rights reserved.)

The key signs and symptoms of vestibular neuritis are rotatory vertigo with an acute onset lasting several days, horizontal spontaneous nystagmus (with a rotational component) toward the unaffected ear, a pathologic head-impulse test toward the affected ear, a deviation of the subjective visual vertical toward the affected ear, postural imbalance with falls toward the affected ear, and nausea. The head-impulse test and caloric irrigation show an ipsilateral deficit of the vestibuloocular reflex. Vestibular neuritis is the third most common cause of peripheral vestibular vertigo. It has an annual incidence of 3.5 per 100,000 population and accounts for 7% of the patients at outpatient clinics specializing in the treatment of vertigo. The reactivation of a latent herpes simplex virus type 1 (HSV-1) infection is the most likely cause, as HSV-1 DNA and RNA have been detected in human vestibular ganglia. Vestibular neuritis is a diagnosis of exclusion. Relevant differential diagnoses are vestibular pseudoneuritis due to acute pontomedullary brainstem lesions or cerebellar nodular infarctions, vestibular migraine, and monosymptomatically beginning Ménière's disease. Recovery from vestibular neuritis is due to a combination of (a) peripheral restoration of labyrinthine function, usually incomplete but can be improved by early treatment with corticosteroids, which cause a recovery rate of 62% within 12 months; (b) mainly somatosensory and visual substitution; and (c) central compensation, which can be improved by vestibular exercise., (Thieme Medical Publishers.)

Vestibular neuritis is the second most common cause of peripheral vestibular vertigo. Its assumed cause is a reactivation of herpes simplex virus type 1 infection. Methylprednisolone significantly improves the recovery of peripheral vestibular function in patients with vestibular neuritis. Clinical studies suggest that specific vestibular exercises improve vestibulo-spinal and vestibulo-ocular compensation in patients with vestibular neuritis. This review discusses the above and comments etiology, epidemiology, pathophysiology, diagnostic procedures and differential diagnosis.

Acute unilateral peripheral and central vestibular lesions can cause similar signs and symptoms, but they require different diagnostics and management. We therefore correlated clinical signs to differentiate vestibular neuritis (40 patients) from central "vestibular pseudoneuritis" (43 patients) in the acute situation with the final diagnosis assessed by neuroimaging. Skew deviation was the only specific but non-sensitive (40%) sign for pseudoneuritis. None of the other isolated signs (head thrust test, saccadic pursuit, gaze evoked nystagmus, subjective visual vertical) were reliable; however, multivariate logistic regression increased their sensitivity and specificity to 92%.

Conclusion: The singular neurectomy as described by Gacek in 1974 is an efficient procedure to control symptoms in case of intractable benign paroxysmal positional vertigo (BPPV), with an acceptable risk of postoperative sensorineural hearing loss (SNHL). We postulate that this complication may not be a direct consequence of the surgical procedure but rather may be consecutive to the reactivation of the biological phenomenon that caused the BPPV. We also observed in one patient that BPPV may exist although no nystagmus can be elicited by provocative manoeuvres., Objective: To report our experience of the surgery, and to analyse the rate and causes of complications., Patients and Methods: The eight patients operated in the department between August 1997 and April 2006 were evaluated in June 2006. One had been operated because he had a typical history of BPPV, but no nystagmus could be elicited by the Hallpike's manoeuvre., Results: All patients were free of vertigo and considered their quality of life improved. The Hallpike's manoeuvre was negative in all cases. A SNHL occurred in two patients, immediately after surgery in one and several months later in the second. The patient with a negative Hallpike's manoeuvre before surgery went back to work 3 weeks after surgery.

Conclusion: Vertigo, defined as an illusion of unequivocal rotatory motion, is a common symptom in the general population that frequently requires individuals to seek medical attention in a primary care centre., Objectives: To evaluate the annual incidence of patients who suffer vertigo, and to examine some of the variables associated, in a sample of the general population of the Autonomic Region of Valencia, Spain., Subjects and Methods: The study was designed as an observational, incidence study. The study area included six primary care centres with a total population of 10760 inhabitants. The parameters studied were age, sex, working status, de novo presentation or recurrent vertigo crisis., Results: A total of 191 patients (17.8 patients per 1000 inhabitants) sought medical attention because of vertigo over the year of the study. Of these, 82 patients (7.6 per 1000 inhabitants) experienced vertigo for the first time, a de novo crisis. Women were more often affected and the crises occurred more frequently in individuals between 50 and 60 years of age. The work status had influence on the results obtained.

Symptoms such as vertigo and unsteady gait occur in various diseases and are among the relatively common chief complaints. Even at present, the mechanisms underlying these disorders are unclear. We considered the possibility of peripheral vestibular disorders correlating with lifestyle-related illnesses. Under these circumstances, we assessed correlations of lifestyle-related illness as background factors for peripheral vestibular disorders and associated arteriosclerotic changes. Using carotid ultrasonography, we assessed maximum intima-media thickness (max IMT) and maximum common carotid artery IMT and evaluated biochemical examinations in 85 patients with peripheral vertigo. The patients were divided into two groups: those with benign paroxysmal positional vertigo (BPPV) and those with peripheral vestibular disorders. The frequency of abnormal IMT was significantly higher in those in the BPPV group. Calculating for average age, max IMT was significantly higher in the BPPV group. The correlation coefficient between age and max IMT was 0.343 (p < .001). All other correlation coefficients also reached statistical significance. Our results indicate that cervical ultrasonography is useful for noninvasive examination of arteriosclerotic changes in patients with peripheral vestibular disorders. Our results also indicated that peripheral vestibular disorder patients show progression of arteriosclerotic changes.

Objective: The aim of this study was to evaluate the audiovestibular disturbance in patients with systemic lupus erythematosus (SLE)., Study Design and Setting: Twenty-eight patients with SLE and 28 healthy control subjects were included. Pure-tone audiometry, impedance audiometry, and electronystagmography (ENG) were used for baseline evaluation. Laboratory tests were carried out. Cranial and brain stem magnetic resonance imagings (MRI) were undertaken., Results: Nineteen (67%) patients reported audiovestibular symptoms. Sensorineural hearing loss was found in 6 (21%) patients. Abnormal results on ENG were significantly higher (50%) (P < 0.01). Abnormal laboratory data were available from 26 patients (P < 0.05). MRI did not show any pathosis., Conclusion: The audiovestibular disturbances in SLE are more prevalent than previously recognized. Although no cause and effect relationship can be established by this type of study, it appears that a relationship exists., Significance: Audiologic research should be directed toward routine, pure tone audiometry, and ENG assessment for patients with SLE to enable crucial treatment.

Hypothesis: Anatomic differences may render the superior division of the vestibular nerve more susceptible to injury during vestibular neuritis., Background: Neural degeneration has been identified in temporal bone studies of vestibular neuritis. Previous anatomic and physiologic studies of vestibular neuritis have demonstrated that the superior division of the vestibular nerve is preferentially affected, with sparing of the inferior division. A preliminary temporal bone study has implicated neural entrapment as a possible cause for this preferential injury., Methods: Two independent unbiased observers performed histologic analysis of 184 temporal bones from our temporal bone library. Measurements of the medial, midpoint, and lateral portions of the superior vestibular, inferior vestibular, and the singular nerves and their bony channels lateral to the internal auditory canal were made. These measurements included the length and width of each bony channel and an estimated percent of each channel occupied by bony spicules at each location., Results: The lengths of the bony channels of the singular nerve (0.598 mm) and the inferior vestibular nerve (0.277 mm) were significantly shorter than the average length of the superior vestibular channel (1.944 mm; p < 0.0001). The total percent of the channel occupied by bone at the midpoint was significantly greater for the superior vestibular (28%) compared with either the singular (0%) or the inferior vestibular channel (18%) (p < 0.0001)., Conclusion: The lateral bony channel of the superior vestibular nerve is seven times longer than the inferior vestibular and more than three times longer than the singular channel. There are a larger percentage of bony spicules occupying the superior vestibular compared with the inferior vestibular or singular channels. In addition, the superior nerve passes through a longer area of severe narrowing compared with the inferior or singular nerves. This anatomic arrangement of a longer bony channel with more interspersed bony spicules could make the superior vestibular nerve more susceptible to entrapment and ischemia.

The purpose of this study was to determine the prevalence of reduced or absent labyrinthine reactivity (vestibulopathy) in two groups of participants with posterior canal BPPV. One group had prior diagnosis of otologic disease (positive history group). No one in the second group had ever been diagnosed with otologic disease (negative history group). Caloric responses were retrospectively analyzed for the two groups. Patients with a positive history exhibited a greater prevalence of vestibulopathy than patients with a negative history. The positive history group, on average, also exhibited a larger unilateral weakness than those patients in the negative history group. We conclude that patients with BPPV and a history of otologic disease are more likely to present with vestibulopathy, than patients with BPPV and no history of otologic disease. This finding supports the benefit of complete vestibular evaluation in patients with BPPV to ensure comprehensive and successful treatment outcome.

Vestibular neuritis presents as sudden unilateral vertigo in the absence of hearing loss or neurologic involvement and is thought to be due to neurotropic viruses. Its morbidity is unknown and it affects both sexes equally, with the highest incidence at 40-50 years of age. The etiology of this condition has been ascribed to viral, bacterial and protozoan infections, as well as allergic and auto-immune causes. Inflammation of the vestibular nerve is followed by demyelination and loss of function, which is not always reversible. Higher plasma fibrinogen and CRP levels in the acute phase, longer BERA latency and I-III interval and increased gadolinium uptake in the vestibular nerve and Scarpa's ganglion on enhanced MRI confirm the inflammatory nature of the process. An animal model of vestibular neuritis using retroauricular inoculation of herpes simplex virus in mice, histologic findings in the temporal bone of individuals who had vestibular neuritis, and influenza A virus infection in cultured Schwann's cells suggest viral infection as the main aetiologic cause.

During the acute phase, symptomatic treatment is practically the only option, and a wide variety of drugs are available. For years, much has been focused on the possibility of using corticosteroids in the treatment of vestibular neuritis. Clearly, if we suspect an inflammatory cause, a treatment that reduces that inflammatory process would, if not reduce the severity of the attack, at least help recovery. If the different studies on this matter failed to concord in many aspects, they do however agree that the use of corticosteroids in the acute phase entails long term beneficial effects for the recovery of vestibular function and allows for a better vestibular compensation. The second part of the treatment is the rehabilitation. In my experience most of the patients undergo a spontaneous vestibular compensation in a short time. Nevertheless, some exercises of visual fixation while the patient is still bed-ridden, can accelerate the recovery process. Those patients, in whom certain instability persists, who are too anxious after their experience or those who will demand this type of treatment, are candidates to undergo a rehabilitative vestibular program. In this paper I will comment on the instrumental and non-instrumental techniques that I use in my daily practice.

Background: Dizziness is a common symptom which is frequently due to either peripheral or central vestibular dysfunction. However, some patients may lack typical signs suggesting a vestibular or cerebellar lesion and they mostly complain of vertigo or posture imbalance induced by visual stimulation. The symptoms immediately improve either on cessation of the visual input or upon closure of the eyes. Such a presentation is typical of visual vertigo., Patients and Methods: From 1993 to 2003, 242 patients were examined for either "vertigo" or "dizziness". The diagnosis of visual vertigo was based on both history and clinical examination and was present in 11 patients., Results: Visual vertigo was diagnosed in 11/242 patients (4.5 %). Age range was 31 - 77 years (mean 47 years) with a sex ratio of 8 females for 3 males. Neuro-ophthalmological examination was normal in all cases., Conclusions: Visual vertigo is not a rare condition but the disease is underdiagnosed. The symptoms result from a mismatch between vestibular, proprioceptive and visual inputs. Neuro-ophthalmological, neurological and neuro-otological examination are often normal or not relevant and the diagnosis is largely based on history. It is important to recognize this entity because the symptoms might improve if the patients are treated with psycho-motor rehabilitation.

The aetiopathogenesis of acute unilateral peripheral vestibular dysfunction (APV), also known as vestibular neuritis, is still debated: the principal cause is viral infection with vascular factors second in importance. Plasmatic D-dimer, considered a plasmatic index of hypercoagulation, was measured in a group of 45 APV patients and in a group of 25 patients suffering from Ménière's disease. Measurements were taken both during the acute stage and after a four to six week period of pharmacological washout. The mean D-dimer levels were significantly higher than those measured in the controls both during the acute phase (301 SD161 vs 202 SD113 ng/mL) and after follow up (304 SD211 vs 192 SD111 ng/mL) (p = 0.008). Moreover, during the acute stage 23 of the APV patients (51.1 per cent) had plasmatic D-dimer levels above the upper normal limit (i.e.: <300 ng/mL), compared to four of those with Ménière's disease (16 per cent). Our results lead us to postulate an involvement of the haemostatic system in APV.

Background: Lyme disease has been described as one possible cause of sudden sensorineural hearing loss and vestibular neuronitis. The necessity of serological diagnosis and its therapeutic consequences have been discussed controversially., Patients and Methods: 344 patients with acute sensorineural hearing loss and 66 patients with vestibular neuronitis were examined in retrospect. By means of ELISA (Enzygnost Borreliosis, Dade Behring Marburg) the specific prevalences of IgG- and IgM-antibodies against borrelia in serum were evaluated. The frequency of seroprevalences for both diseases were compared to those given in the literature. Neurootological findings of the seropositive patients were compared with those of seronegative and analysed statistically., Results: 15.7 % of the patients with sudden sensorineural hearing loss had positive levels of IgG-antibodies. IgM-titers were elevated in 4.7 % of the patients. The seroprevalences for IgM and IgG were above those described by other investigators for the healthy population. Patients with positive IgM-antibodies showed more often low frequency hearing loss than IgG-positive patients. 18.2 % of the patients with neuronitis vestibularis had IgG- and 1.5 % IgM-antibodies against Borrelia. Whereas IgG occurred more often than known for the healthy population, IgM was within the limit for the healthy population. The seropositive group did not show any remarkable neurootological signs compared with the seronegative group., Conclusions: Because of the elevated seroprevalences Borrelia infections may be one possible but very rare cause of sudden sensorineural hearing loss and vestibular neuronitis. Low frequency hearing loss may be a sign for an infection with Borrelia as an etiological factor especially in combination with seropositive titers. In case of the presence of IgM-antibodies, patients may be treated with oral antibiotics (Doxycyclin, Cefuroxim). In patients with neuronitis vestibularis a neuroborreliosis should be excluded by means of lumbar puncture.

It has taken many decades to arrive at today's concept of cupula mechanics in the stimulation of endolymphatic flows on the hair cells in the ampullae of the semicircular canal. While Steinhausen assumed free swing-door movement of the cupula in the 1930s, Hillman was the first to demonstrate firm cupula attachment to the ampulla wall as a physiological necessity in the 1970s. In contrast to the present clinical concepts of acute peripheral vestibular functional disorders (circulatory disturbances, viral or bacterial infection, altered electrolytes in the endolymph), this study examines the extent to which an impaired attachment mechanism can trigger peripheral vestibular disorders. For this purpose, we used a pigeon model (n = 8), in which mechanical detachment of the cupula from the ampulla wall was achieved by means of a targeted pressure increase in the ampulla of the lateral semicircular canal. In two additional animals the labyrinth was completely destroyed on one side in order to directly compare partial and complete vestibular disorders. In this way partial damage to the lateral semicircular canal ampulla presents a clinical picture whose symptoms are very similar to those of an idiopathic vestibular disorder in humans. Their intensity and course of compensation differ markedly from the symptoms of complete vestibular destruction. Subsequent histological examination revealed that the hair cells remained intact during the experimental detachment of the cupula. Our results thus show that only altered cupula mechanics seem to trigger the clinical picture of a peripheral vestibular disorder. This may result in completely new approaches to differential diagnosis and the therapy of vestibular neuronitis.