We sought to investigate the utility of new non-invasive tests of semicircular-canal and otolith function that are usable in the neuro-otology office practice in patients with vestibular schwannoma. Fifty patients with vestibular schwannoma were assessed using a 5-item battery consisting of air-conducted cervical- and bone conducted ocular-vestibular-evoked myogenic potentials (AC cVEMPs and BC oVEMPs) and video head impulse testing (vHIT) in all three canal planes. VEMP asymmetry ratios, latencies, and vHIT gains were used to determine the test sensitivity, relationship with tumour size and the pattern of vestibular nerve involvement. The percentage of abnormalities for each of the five tests for the entire sample ranged between 36.2-61.7%. In 58.3 % of patients, test abnormalities were referable to both superior and inferior vestibular nerve divisions. Selective inferior nerve dysfunction was identified in 10.4% and superior nerve dysfunction in 12.5%. The remaining 18.8% of patients demonstrated a normal test profile. The sensitivity of the 5-item battery increased with tumour size and all patients with medium to large (>14 mm) schwannoma had at least two abnormal vestibular test result. Our results indicate that dysfunction of the superior and inferior vestibular nerve evolves in parallel for most patients with schwannoma. Unexplained vHIT and VEMP asymmetry should alert otologists and neurologists to undertake imaging in patients presenting with non-specific disequilibrium or vertigo.

As the number of cochlear implants increase and patients outlive the lifespan of their devices, we will face a growing number of revision procedures. Audiologists and otologists should be competent in diagnosing and managing device failure and medical complications requiring cochlear re-implantation.

The normal vestibulo-ocular reflex (VOR) generates almost perfectly compensatory smooth eye movements during a 'head-impulse' rotation. An imperfect VOR gain provokes additional compensatory saccades to re-acquire an earth-fixed target. In the present study, we investigated vestibular and visual contributions on saccade production. Eye position and velocity during horizontal and vertical canal-plane head-impulses were recorded in the light and dark from 16 controls, 22 subjects after complete surgical unilateral vestibular deafferentation (UVD), eight subjects with idiopathic bilateral vestibular loss (BVL), and one subject after complete bilateral vestibular deafferentation (BVD). When impulses were delivered in the horizontal-canal plane, in complete darkness compared with light, first saccade frequency mean(SEM) reduced from 96.6(1.3)-62.3(8.9) % in BVL but only 98.3(0.6)-92.0 (2.3) % in UVD; saccade amplitudes reduced from 7.0(0.5)-3.6(0.4)˚in BVL but were unchanged 6.2(0.3)-5.5(0.6)˚in UVD. In the dark, saccade latencies were prolonged in lesioned ears, from 168(8.4)-240(24.5) ms in BVL and 177(5.2)-196(5.7) ms in UVD; saccades became less clustered. In BVD, saccades were not completely abolished in the dark, but their amplitudes decreased from 7.3-3.0˚and latencies became more variable. For unlesioned ears (controls and unlesioned ears of UVD), saccade frequency also reduced in the dark, but their small amplitudes slightly increased, while latency and clustering remained unchanged. First and second saccade frequencies were 75.3(4.5) % and 20.3(4.1) %; without visual fixation they dropped to 32.2(5.0) % and 3.8(1.2) %. The VOR gain was affected by vision only in unlesioned ears of UVD; gains for the horizontal-plane rose slightly, and the