LAUSR

Since the first descriptions of superior canal dehiscence (SCD) syndrome, it has been widely demonstrated how a bony defect overlying the superior semicircular canal (SSC) can result in a low-impedance pathway for sound and pressure stimuli, resulting in a variety of audio-vestibular symptoms and signs consistent with a third window mechanism [1–3]. Although physiologists and clinicians have clearly explained the mechanisms accounting for both low-frequencies conductive hearing loss on audiometry and enhanced amplitudes of vestibular-evoked myogenic potentials (VEMPs), mismatching results have been achieved in the interpretation of the vestibulo-ocular reflex (VOR) data for the affected SSC. In fact, whilst it has been reported how sound and/or pressure stimuli can result in eye movements aligning with the plane of the dehiscent SSC [1,2,4], studies performed either with magnetic-scleral search coils [2,5] or with the video-head impulse test (vHIT) [6,7] observed that VOR-gain values for the affected SSC could be impaired. These questions have strongly arisen thanks to the growing accessibility of canal VOR-gain measurements in the highfrequency domain promoted by the recent introduction of the vHIT in clinical practice. Our aim is to point out some aspects resulting from our clinical experience in this field, and to offer further possible interpretations for some apparently mismatching data with a common theory accounting for overall measurements of SSC activity in case of SCD.