Dear Sir,It is difficult to obtain objective measures of vestibularfunction from very young children (3- to 7-years-old)because they are unwilling to receive caloric tests whichinduce vertigo, or to undergo bedside examination forspontaneous nystagmus as they must be in darkness forsome minutes [1, 2]. It is also difficult to obtain an accuratemedical history in such young patients in a subacute stage,and in order to understand what really happened, the cli-nician relies on the story told by the parents. These diffi-culties increase when a child comes to a vertigo clinic or anEmergency Department in the acute stage of a vertigoattack complaining that the world is turning around. Underthese circumstances, a clinician can identify the classicalsigns and symptoms which are dependent on the absentfunction of the affected vestibular labyrinth. Such classicalstatic clinical signs are (a) spontaneous nystagmus with thequick phase of the horizontal component directed awayfrom the affected ear, (b) ocular torsion with both eyesrolled away from the affected ear indicating unilaterallyreduced otolithic function of the affected ear, (c) skewdeviation with a vertical misalignment between the twoeyes such that the ipsilesional eye shows a lower positionin the orbit, (d) postural instability with sensations offalling toward the lesioned side, related to reduced functionof the affected ear projecting to ipsilateral vestibulo-spinalresponses. The usual standard tests of dynamic vestibularfunction are (e) the Hallpike–Fitzgerald canal paresismeasure from caloric testing and (f) the clinical sign ofcanal paresis (the head-impulse sign)—during brief, pas-sive, unpredictable, horizontal head turns toward theaffected ear, the patient with reduced unilateral horizontalcanal function fails to maintain fixation on an earth-fixedtarget and so makes corrective (overt) saccades at the endof the head rotation in order to regain fixation [3]. Duringsimilar rotations toward the healthy ear no overt saccadesare evident. The overt saccade is a sign of reduced dynamichorizontal canal function; however, this clinical sign issubjective, in that there is no objective measure of the headvelocity stimulus or the eye velocity response and so noobjective measure of vestibulo-ocular (VOR) gain.Three new objective measures of dynamic vestibularfunction have been reported. These tests are quick, accurateand not demanding for the patients (i.e., they do not inducevertigo), and above all they can be used to obtain objectivemeasures of the dynamic function of all the vestibularreceptors, both semicircular canals and otoliths, even invery young children. Two of the tests use vestibular-evoked myogenic potentials to sound and vibration. Thefirst is the cervical vestibular-evoked myogenic potential(cVEMP) to air-conducted sound (ACS) or bone conductedvibration (BCV) [4, 5]. These stimuli have been shown topreferentially activate otolith irregular afferents from theutricular and saccular macula [5–7]. The cVEMP responseto ACS and BCV indicates dynamic saccular and inferiorvestibular nerve function. In healthy subjects with surfaceelectrodes on the tensed sternocleidomastoid muscles, it isfound that that in response to BCV or intense ACS stim-ulation there is a short-latency positive (inhibitory) poten-tial (p13-n23) at a latency of around 13 ms from stimulusonset, indicating ipsilateral saccular function. The second