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

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.

Keywords: high frequencies; nystagmus; skull vibration; vertigo; vestibular disease.

Figure 1

Skull vibration-induced nystagmus test technique in clinical practice. (A) Principle of stimulation: the examiner can face the subject, as in the first example. The vibrator cylindrical contact is applied perpendicularly to the designated surface (red spot) with a pressure of about 10 N or 1 kg on the vertex or each mastoid process [level to the external acoustic meatus (Green spot)]. The examiner uses the other hand to maintain and immobilize the subject’s head. The same type of stimulation can be performed with the examiner behind the subject (second example situation). Stimulation must avoid the mastoid tip to prevent from muscular vibration radiation and proprioceptive involvement. (B) Mastoid stimulation; examiner in front of the subject; the other hand immobilizes the head. 3F Synapsys stimulator (France). Videonystagmoscopic recording (Collin ORL, France).

Figure 2

Topographic optimization analysis of the skull vibration-induced nystagmus test. (A) Procedure. (B) Results: the piezoelectric potentials (millivolts) recorded on the mastoid are significantly different according to the location of the stimulation (Friedman test, P < 0.001): the values obtained during the vibratory stimulation of the contralateral mastoid are higher than those obtained after vertex or ipsilateral and contralateral posterior cervical muscle vibrations (Wilcoxon tests, P < 0.001). No difference is observed between vertex and posterior cervical muscle stimulation locations (Wilcoxon tests, P > 0.05). The piezoelectric potentials recorded on the vertex or the posterior cervical muscles are not different according to the location of the stimulation (Friedman test and Wilcoxon test, P > 0.05).

Figure 3

Example of 3D recordings in a total unilateral vestibular lesion—vibration-induced nystagmus (VIN) onset and offset. Left total unilateral vestibular loss 3D recording (translabyrinthine surgery performed 10 years ago) for vestibular schwannoma. The recordings are successively performed on the right mastoid (RM), the left mastoid (LM) with a camera on the right eye (RE) or the left eye (LE). The VIN is repeatable, reproducible on both mastoids in the same direction, beats away from the lesion side, starts and stops with the stimulation and presents no secondary reversal. H, horizontal component; V, vertical component; T, torsional component; N, no stimulus.

Figure 4

Partial unilateral vestibular lesions [vibration-induced nystagmus (VIN) 2D recording]. (A) Example of right vestibular neuritis or acute peripheral vestibular disorder (APVD). Direct recording of head-shaking-nystagmus (HSN) and VIN at 30, 60, and 100 Hz. When skull vibration-induced nystagmus test (SVINT) is performed after the HST, it is recommended to observe an interval between the two tests (about 2 min) to avoid interference of HSN on VIN due to a possible second HSN reversal phase. (B) Same patient, right APVD: recording of the eye slow-phase velocity (SPV). (C) Right chemical labyrinthectomy (intratympanic gentamicin): 2D recording of the VIN SPV; SVINT 30 Hz [right mastoid (RM)–left mastoid (LM)]; 60 Hz (RM–LM); 100 Hz (RM–LM) protocol.

Figure 5

Skull vibration-induced nystagmus test (SVINT) is more sensitive to identify peripheral than central diseases. Comparative sensitivity of caloric test (CaT), SVINT, and head-shaking test (HST) in populations of total unilateral vestibular lesions (tUVL) (n = 131), of partial unilateral vestibular lesions (pUVL) (n = 78), and brainstem lesions (BSL) (n = 36). SVINT is more sensitive to reveal peripheral than central lesions (P = 0.04).

Figure 6

Results in conductive hearing loss observed in unilateral SCD and otosclerosis (OS). Vibration-induced nystagmus (VIN) acts as a vestibular Weber Test. Skull vibration-induced nystagmus test (SVINT)—percentages (with 95% confidence interval) of no VIN, VIN beating toward the healthy side, and VIN beating toward the lesion side (A) and median (with interquartile range) of the slow-phase velocity of the VIN (B) observed in superior canal dehiscence (SCD) and otosclerosis (OS) patients (**P < 0.001, ***P < 0.0001).

Figure 7

Vibration-induced nystagmus complements other vestibular tests in the vestibule multifrequency analysis. Place of the SVINT in the currently known frequency spectrum of the vestibular system. This graph summarizes the complementarity of vestibular tests, introduces the concept of the optimal vestibular compensation zone for the horizontal canal and the bone conduction stimulation frequencies necessary to obtain ocular vestibular-evoked myogenic potentials and cervical evoked myogenic potentials (cVEMP) (EMG). Adapted from Chays et al. (72) modified by Dumas (university PhD thesis 2014) (73). VLF, very low frequencies; LF, low F; MF, middle F: HF, high F; VHF, very high F.

Figure 8

Angular velocity data and the response to low-frequency bone-conducted vibration for an anterior semicircular canal unit. (Bottom panel) Neural activation by angular acceleration, identifying the afferent is a canal neuron. (Top Panel) Response of the same unit to bone-conducted vibration at 200 (left) and 150 Hz (right). As stimulus frequency is decreased the neuron shows increased firing—at 200 Hz there is a modest response during the stimulus but at 150 Hz there is a strong increase in firing tightly locked to the onset and offset of the brief stimulus.