Vestibular Nucleus Involvement in Patients With Acute Vertigo Due to Herpes Zoster Oticus or Vestibular Neuritis.

OBJECTIVES: Herpes zoster oticus (HZO) typically provokes vestibular symptoms and is traditionally viewed as a cranial nerve equivalent of shingles, but in contrast to vestibular neuritis (VN), it is unclear whether the pathology of HZO is limited to the vestibular nerve (neuritis) or can also involve the brainstem (nucleitis). METHODS: We retrospectively compared brain MRIs of patients with HZO with those of patients with VN to study radiologic changes in the brainstem. RESULTS: Five of 10 patients with HZO showed signal abnormalities in the vestibular nuclei, which lie in multiple vascular territories, whereas no patients with VN exhibited such findings. DISCUSSION: HZO may at least in part reflect vestibular nucleitis, as opposed to a pure neuritis.

Universal Repositioning Maneuver: A New Treatment for Single Canal and Multi-Canal Benign Paroxysmal Positional Vertigo by 3-Dimensional Model Analysis.

BACKGROUND: Benign paroxysmal positional vertigo is the most common peripheral vestibular disorder and is currently treated by many types of repositioning maneuvers. A simplification of this procedure would be desirable. A new, anatomically realistic, 3-dimensional computational simulator of the human labyrinth provides a novel insight to evaluate the viability of any new maneuver. The purpose of this study is to propose a single maneuver with potential to treat canalolithiasis-type benign paroxysmal positional vertigo of any individual canal, or even multiple canals on the same side, based on a 3-dimensional model. METHODS: The benign paroxysmal positional vertigo Viewer, a 3-dimensional model of the human labyrinth, was used to analyze a "Universal Repositioning Maneuver." RESULT: Through the gravity vector, the expected position of the otoliths was demonstrated by moving the model through a single sequence of head positions, successfully promoting otolith migration from the three semicircular canals to the utricular cavity, either individually or together. CONCLUSION: The analysis with the 3-dimensional model predicts the effectiveness of the Universal Repositioning Maneuver for the resolution of each single canal or multiple-canal benign paroxysmal positional vertigo canalolithiasis, making treatment much more straightforward.

When, where, and why should we look for vestibular dysfunction in people with diabetes mellitus?

The biochemistry of diabetes mellitus results in multi-system tissue compromise that reduces functional mobility and interferes with disease management. Sensory system compromise, such as peripheral neuropathy and retinopathy, are specific examples of tissue compromise detrimental to functional mobility. There is lack of clarity regarding if, when, and where parallel changes in the peripheral vestibular system, an additional essential sensory system for functional mobility, occur as a result of diabetes. Given the systemic nature of diabetes and the plasticity of the vestibular system, there is even less clarity regarding if potential vestibular system changes impact functional mobility in a meaningful fashion. This commentary will provide insight as to when we should employ diagnostic vestibular function tests in people with diabetes, where in the periphery we should look, and why testing may or may not matter. The commentary concludes with recommendations for future research and clinical care.

The Role of the Smartphone in the Diagnosis of Vestibular Hypofunction: A Clinical Strategy for Teleconsultation during the COVID-19 Pandemic and Beyond.

Introduction Vestibular disorders (VDs) are highly prevalent in primary care. Although in general they comprise conditions that are not life-threatening, they are associated with significant functional and physical disability. However, the current coronavirus disease 2019 (COVID-19) pandemic has imposed limitations on the standard treatment of benign conditions, including VDs. In this context, other resources may aid in the diagnosis and management of patients with VDs. It is well known that teleconsultation and teletreatment are both safe and effective alternatives to manage a variety of conditions, and we maintain that VDs should be among these. Objective To develop a preliminary model of clinical guidelines for the evaluation by teleconsultation of patients with suspected diagnosis of vestibular hypofunction during the COVID-19 pandemic and beyond. Methods A bibliographic review of the diagnostic feasibility in VDs by teleconsultation was carried out in the LILACS, SciELO, MEDLINE, and PubMed databases; books and specialized websites were also consulted. The legal, regulatory, and technical issues involving digital consultations were reviewed. Results We found 6 field studies published between 1990 and 2020 in which the efficiency of teleconsultations was observed in the contexts of epidemics and environmental disorders and disadvantageous geographical conditions. After reviewing them, we proposed a strategy to examine and address vestibular complaints related to vestibular hypofunction. Conclusion The creation of a digital vestibular management algorithm for the identification, counseling, initial intervention, monitoring and targeting of people with possible vestibular hypofunction seems to be feasible, and it will provide a reasonable alternative to in-person evaluations during the COVID-19 pandemic and beyond.

The Enduring Controversy of Cervicogenic Vertigo, and Its Place among Positional Vertigo Syndromes.

The idea of cervicogenic vertigo (CV) was proposed nearly a century ago, yet despite considerable scrutiny and research, little progress has been made in clarifying the underlying mechanism of the disease, developing a confirmatory diagnostic test, or devising an appropriately targeted treatment. Given the history of this idea, we offer a review geared towards understanding why so many attempts at clarifying it have failed, with specific comments regarding how CV fits into the broader landscape of positional vertigo syndromes, what a successful diagnostic test might require, and some practical advice on how to approach this in the absence of a diagnostic test.

Vestibular Testing.

PURPOSE OF REVIEW: Vestibular testing, both at the bedside and in the laboratory, is often critical in diagnosing patients with symptoms of vertigo, dizziness, unsteadiness, and oscillopsia. This article introduces readers to core concepts, as well as recent advances, in bedside and instrumented vestibular assessments. RECENT FINDINGS: Vestibular testing has improved immensely in the past 2 decades. While history and bedside testing is still the primary method of differential diagnosis in patients with dizziness, advances in technology such as the ocular vestibular-evoked myogenic potential test for superior canal dehiscence and the video head impulse test for vestibular neuritis have capabilities that go far beyond the bedside examination. Current vestibular testing now allows clinicians to test all five vestibular sensors in the inner ear. SUMMARY: Contemporary vestibular testing technology can now assess the entire vestibular periphery. Relatively subtle conditions, such as superior canal dehiscence or a subtle vestibular neuritis, can now be diagnosed with far greater certainty.

The spectrum of acute vestibular neuropathy through modern vestibular testing: A descriptive analysis.

OBJECTIVE: Acute vestibular neuropathy (AVN), often referred to as vestibular neuritis, is a cranial neuropathy responsible for a significant proportion of cases of acute vertigo. This study describes the spectrum of lesion patterns in AVN as identified by video head impulse testing (vHIT) which assesses the high frequency vestibulo-ocular reflex function of the semicircular canals, and cervical and ocular vestibular evoked myogenic potentials (VEMPs) which assess otolith function. METHODS: We used vHIT and VEMPs to assess 35 patients with vestibular neuropathy in the acute stage. RESULTS: Unilateral superior division vestibular nerve involvement was the most common variant (57.1%), followed by unilateral superior and inferior division (28.5%), bilateral superior division (8.5%) and unilateral inferior division (5.7%). We observed a partial inverse correlation between the proportion of afferent fibers from an organelle, and the likelihood that the test of that organelle's function will be abnormal. CONCLUSION: vHIT and VEMPs provide more detailed characterization of lesion pattern in AVN than caloric testing. SIGNIFICANCE: Comparison of lesion patterns from neuro-physiological testing with what is known about the proportional distribution of afferent fibers from the vestibular end-organelles suggests a new, neuro-anatomically based insight regarding susceptibility of these pathways to AVN.

Histology and neuroanatomy suggest a unified mechanism to explain the distribution of lesion patterns in acute vestibular neuropathy.

Human temporal bone studies have described the distribution of afferent fibers from each of the five organelles in the labyrinth. Data from vestibular tests in patients with vestibular neuritis can be abnormal in almost any pattern. We propose a unified explanation for these patterns, based on histological and neuroanatomical factors.

Migraine Associated Vertigo.

This chapter is a brief overview of migraine associated vertigo (MAV), focusing on the points most relevant to the practicing clinician. We review the definition of MAV, theories regarding its underlying pathophysiology, clinical presentation, epidemiology, findings on physical examination and oto vestibular testing, differential diagnosis, management and prognosis.

Utricular function in vestibular neuritis: a pilot study of concordance/discordance between ocular vestibular evoked myogenic potentials and ocular cycloposition.

Vestibular neuritis (VN) can affect utricular afferents. Utricular function can be assessed by ocular vestibular evoked myogenic potentials (oVEMPs) whose abnormalities include weak or absent responses, and ocular cycloposition whose abnormalities include ocular torsion (OT). When studied independently in vestibular neuritis, oVEMPs are abnormal in 61-82% of cases, and OT is present in 72-80% of cases. The similar range of abnormalities suggests the hypothesis that these tests should be concordantly abnormal. We tested this hypothesis by identifying consecutive adult cases of VN in whom both oVEMPs and OT were performed. OT and oVEMP overlapped (both were abnormal) in only 47% of cases. In 40% of cases oVEMPs alone were abnormal, and in 13% of cases, OT alone was present. These results suggest that oVEMPs and OT assess different aspects of utricular function believed to arise from discrete zones of the utricular macula; the former are thought to reflect the activity of extra-striolar afferents (which detect constant acceleration), and the latter reflects the activity of striolar afferents (which detect change in acceleration).

The Gain-Time Constant Product Quantifies Total Vestibular Output in Bilateral Vestibular Loss.

Patients with inner ear damage associated with bilateral vestibular impairment often ask "how much damage do I have." Although there are presently three clinical methods of measuring semicircular canal vestibular function; electronystagmography (ENG or VENG), rotatory chair and video head-impulse (VHIT) testing; none of these methods provides a method of measuring total vestibular output. Theory suggests that the slow cumulative eye position can be derived from the rotatory chair test by multiplying the high frequency gain by the time constant, or the "GainTc product." In this retrospective study, we compared the GainTc in three groups, 30 normal subjects, 25 patients with surgically induced unilateral vestibular loss, and 24 patients with absent or nearly absent vestibular responses due to gentamicin exposure. We found that the GainTc product correlated better with remaining vestibular function than either the gain or the time constant alone. The fraction of remaining vestibular function was predicted by the equation R = (GainTc/11.3) - 0.6. We suggest that the GainTc product answers the question "how much damage do I have," and is a better measure than other clinical tests of vestibular function.

Bilateral Vestibular Weakness.

Bilateral vestibular weakness (BVW) is a rare cause of imbalance. Patients with BVW complain of oscillopsia. In approximately half of the patients with BVW, the cause remains undetermined; in the remainder, the most common etiology by far is gentamicin ototoxicity, followed by much rarer entities such as autoimmune inner ear disease, meningitis, bilateral Ménière's disease, bilateral vestibular neuritis, and bilateral vestibular schwannomas. While a number of bedside tests may raise the suspicion of BVW, the diagnosis should be confirmed by rotatory chair testing. Treatment of BVW is largely supportive. Medications with the unintended effect of vestibular suppression should be avoided.

Bilateral vestibular loss.

Bilateral vestibular loss is a rare cause of visual disturbance (oscillopsia) and imbalance. When severe, the most common cause is iatrogenic-gentamicin ototoxicity. Bilateral loss is easily diagnosed at the bedside with the dynamic illegible E test. If this test is omitted, it can easily be misdiagnosed as a cerebellar syndrome. Treatment is largely supportive. Care should be taken to avoid medications that suppress vestibular function, and to encourage activity.

Migraine-associated vertigo.

This article presents a brief overview of migraine-associated vertigo for the practicing otolaryngologist. Discussion includes the definition of migraine-associated vertigo and its pathophysiology, clinical features, demographics, findings on physical examination, use of otologic and vestibular testing, differential diagnosis, treatment, and prognosis.

Infrequent causes of disequilibrium in the adult.

This content focuses on some of the less common causes of dizziness in the adult. The diseases have been divided into the 2 broad categories of those causing chronic symptoms and those causing episodic symptoms. Presented here are the unusual causes of chronic disequilibrium in the adult, including bilateral vestibular loss, progressive supranuclear palsy, spinocerebellar ataxias, and mal de debarquement. Also discussed are the unusual causes of episodic disequilibrium in the adult, including psychogenic disequilibrium, vestibular paroxysmia, episodic ataxia, vestibular seizures, and cervicogenic vertigo.