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      The Skull Vibration-Induced Nystagmus Test of Vestibular Function—A Review

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          Abstract

          A 100-Hz bone-conducted vibration applied to either mastoid induces instantaneously a predominantly horizontal nystagmus, with quick phases beating away from the affected side in patients with a unilateral vestibular loss (UVL). The same stimulus in healthy asymptomatic subjects has little or no effect. This is skull vibration-induced nystagmus (SVIN), and it is a useful, simple, non-invasive, robust indicator of asymmetry of vestibular function and the side of the vestibular loss. The nystagmus is precisely stimulus-locked: it starts with stimulation onset and stops at stimulation offset, with no post-stimulation reversal. It is sustained during long stimulus durations; it is reproducible; it beats in the same direction irrespective of which mastoid is stimulated; it shows little or no habituation; and it is permanent—even well-compensated UVL patients show SVIN. A SVIN is observed under Frenzel goggles or videonystagmoscopy and recorded under videonystagmography in absence of visual-fixation and strong sedative drugs. Stimulus frequency, location, and intensity modify the results, and a large variability in skull morphology between people can modify the stimulus. SVIN to 100 Hz mastoid stimulation is a robust response. We describe the optimum method of stimulation on the basis of the literature data and testing more than 18,500 patients. Recent neural evidence clarifies which vestibular receptors are stimulated, how they cause the nystagmus, and why the same vibration in patients with semicircular canal dehiscence (SCD) causes a nystagmus beating toward the affected ear. This review focuses not only on the optimal parameters of the stimulus and response of UVL and SCD patients but also shows how other vestibular dysfunctions affect SVIN. We conclude that the presence of SVIN is a useful indicator of the asymmetry of vestibular function between the two ears, but in order to identify which is the affected ear, other information and careful clinical judgment are needed.

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          Most cited references76

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          Sound- and/or pressure-induced vertigo due to bone dehiscence of the superior semicircular canal.

          To present symptoms, patterns of nystagmus, and computed tomographic scan identification of patients with sound- and/or pressure-induced vertigo due to dehiscence of bone overlying the superior semicircular canal. To describe anatomical findings and outcome in 2 patients undergoing plugging of the superior semicircular canal for treatment of these symptoms. Prospective study of a case series in a tertiary care referral center. Eight patients with vertigo, oscillopsia, and/or disequilibrium related to sound, changes in middle ear pressure, and/or changes in intracranial pressure were identified in a 2-year period. Seven of these patients also had vertical-torsional eye movements induced by these sound and/or pressure stimuli. The direction of the evoked eye movements could be explained by excitation or inhibition of the superior semicircular canal in the affected ear. Computed tomographic scans of the temporal bones identified dehiscence of bone overlying the affected superior semicircular canal in each case. Disabling disequilibrium in 2 patients prompted plugging of the dehiscent superior canal through a middle cranial fossa approach. Symptoms were improved in each case. One patient developed recurrent symptoms requiring an additional plugging procedure and developed sensorineural hearing loss several days after this second procedure. We have identified patients with a syndrome of vestibular symptoms induced by sound in an ear or by changes in middle ear or intracranial pressure. These patients can also experience chronic disequilibrium. Eye movements in the plane parallel to that of the superior semicircular canal were evoked by stimuli that have the potential to cause ampullofugal or ampullopetal deflection of this canal's cupula in the presence of a dehiscence of bone overlying the canal. The existence of such deshiscences was confirmed with computed tomographic scans of the temporal bones. Surgical plugging of the affected canal may be beneficial in patients with disabling symptoms.
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            Bone-conducted sound: physiological and clinical aspects.

            The fact that vibration of the skull causes a hearing sensation has been known since the 19th century. This mode of hearing was termed hearing by bone conduction. Although there has been more than a century of research on hearing by bone conduction, its physiology is not completely understood. Lately, new insights into the physiology of hearing by bone conduction have been reported. Knowledge of the physiology, clinical aspects, and limitations of bone conduction sound is important for clinicians dealing with hearing loss and is the purpose of this review. The data were compiled from the published literature in the areas of clinical bone conduction hearing, bone conduction hearing aids, basic research on bone conduction physiology, and recent research on bone conduction hearing from our laboratory. Five factors contributing to bone conduction hearing have been identified: 1) sound radiated into the external ear canal, 2) middle ear ossicle inertia, 3) inertia of the cochlear fluids, 4) compression of the cochlear walls, and 5) pressure transmission from the cerebrospinal fluid. Of these five, inertia of the cochlear fluid seems most important. Bone conduction sound is believed to reflect the true cochlear function; however, certain conditions such as middle ear diseases can affect bone conduction sensitivity, but less than for air conduction. The bone conduction route can also be used for hearing aids; since the bone conduction route is less efficient than the air conduction route, bone conduction hearing aids are primarily used for hearing losses where air conduction hearing aids are contraindicated.
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              The interpretation of clinical tests of peripheral vestibular function.

              Recently, new clinical tests of canal and otolith function have been introduced. They rest on sound anatomical and physiological evidence; however, the interpretation of the results of these tests has only recently been clarified. This review summarizes the anatomical and physiological evidence underpinning the tests of both canal and otolith function to provide a full picture of the interpretation of the tests, which allow the clinician to assess the status of the peripheral vestibular function of a patient--all six canals and four otoliths. The present review does not document all the minute details associated with each test, but provides an overview of the interpretation of properly presented tests and shows typical response profiles of patients with various types of vestibular loss, based on published anatomical, physiological, and clinical evidence. Copyright © 2012 The American Laryngological, Rhinological, and Otological Society, Inc.
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                Author and article information

                Contributors
                Journal
                Front Neurol
                Front Neurol
                Front. Neurol.
                Frontiers in Neurology
                Frontiers Media S.A.
                1664-2295
                09 March 2017
                2017
                : 8
                : 41
                Affiliations
                [1] 1Department of Oto-Rhino-Laryngology, Head and Neck Surgery, University Hospital , Grenoble, France
                [2] 2EA 3450 DevAH, Development, Adaptation and Disadvantage, Faculty of Medicine and UFR STAPS, University of Lorraine , Villers-lès-Nancy, France
                [3] 3Vestibular Research Laboratory, School of Psychology, the University of Sydney , Sydney, NSW, Australia
                [4] 4Sports Medicine Research Laboratory, Luxembourg Institute of Health , Strassen, Luxembourg
                [5] 5Department of Paediatric Oto-Rhino-Laryngology, University Hospital of Nancy , Vandoeuvre-lès-Nancy, France
                [6] 6INSERM UMR 2015 , Grenoble, France
                Author notes

                Edited by: Richard Lewis, Harvard University, USA

                Reviewed by: Bernard Cohen, Icahn School of Medicine at Mount Sinai, USA; Shinichi Iwasaki, University of Tokyo, Japan

                *Correspondence: Georges Dumas, GDumas@ 123456chu-grenoble.fr

                Specialty section: This article was submitted to Neuro-otology, a section of the journal Frontiers in Neurology

                Article
                10.3389/fneur.2017.00041
                5343042
                28337171
                c13a47ab-ba56-42b5-80fa-ad19ec81b103
                Copyright © 2017 Dumas, Curthoys, Lion, Perrin and Schmerber.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 18 August 2016
                : 30 January 2017
                Page count
                Figures: 8, Tables: 1, Equations: 0, References: 84, Pages: 18, Words: 11664
                Categories
                Neuroscience
                Review

                Neurology
                skull vibration,nystagmus,vertigo,high frequencies,vestibular disease
                Neurology
                skull vibration, nystagmus, vertigo, high frequencies, vestibular disease

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