Nystagmus goggles: how to use them, what you find and what it means.

A fundamental characteristic of peripheral vestibular nystagmus, in particular horizontal nystagmus, is that it is suppressed by visual fixation. This means that a patient with a vertigo attack of peripheral vestibular origin might have no obvious spontaneous nystagmus on clinical examination. Goggles that reduce or remove visual fixation allow the cliniican to observe nystagmus in this situation. Nystagmus goggles are essential for any clinician dealing with dizzy patients. Here, we discuss why this is so and how easy it is to acquire and use them.

Effect of stimulus rise-time on the ocular vestibular-evoked myogenic potential to bone-conducted vibration.

OBJECTIVES: The negative potential at 10 msec (called n10) of the ocular vestibular-evoked myogenic potential (oVEMP) recorded beneath the eyes in response to bone-conducted vibration (BCV) delivered to the skull at the midline in the hairline (Fz) is a new indicator of otolithic, and in particular utricular, function. Our aim is to find the optimum combination of frequency and rise-time for BCV stimulation, to improve the sensitivity of oVEMP testing in the clinic. DESIGN: We tested 10 healthy subjects with 6 msec tone bursts of BCV at three stimulus frequencies, 250, 500, and 750 Hz, at rise-times ranging between 0 and 2 msec. The BCV was delivered at Fz. RESULTS: The n10 response was significantly larger at the shorter rise-times, being largest at zero rise-time. In addition, we examined the effect of stimulus frequency in these same subjects by delivering 6 msec tone bursts at zero rise-time at a range of frequencies from 50 to 1200 Hz. The main effect of rise-time was significant with shorter rise-times leading to larger n10 responses and the Rise-Time × Frequency interaction was significant so that at low frequencies (100 Hz) shorter rise-times had a modest effect on n10 whereas at high frequencies (750 Hz) shorter rise-times increased n10 amplitude substantially. The main effect of frequency was also significant: The n10 response tended to be larger at lower frequency, being largest between 250 and 500 Hz. CONCLUSIONS: In summary, in this sample of healthy subjects, the most effective stimulus for eliciting oVEMP n10 to BCV at Fz was found to be a tone burst with a rise-time of 0 msec at low stimulus frequency (250 or 500 Hz).

A review of the geometrical basis and the principles underlying the use and interpretation of the video head impulse test (vHIT) in clinical vestibular testing.

This paper is concerned mainly with the assumptions underpinning the actual testing procedure, measurement, and interpretation of the video head impulse test-vHIT. Other papers have reported in detail the artifacts which can interfere with obtaining accurate eye movement results, but here we focus not on artifacts, but on the basic questions about the assumptions and geometrical considerations by which vHIT works. These matters are crucial in understanding and appropriately interpreting the results obtained, especially as vHIT is now being applied to central disorders. The interpretation of the eye velocity responses relies on thorough knowledge of the factors which can affect the response-for example the orientation of the goggles on the head, the head pitch, and the contribution of vertical canals to the horizontal canal response. We highlight some of these issues and point to future developments and improvements. The paper assumes knowledge of how vHIT testing is conducted.

The Relationship between the Subjective Visual Horizontal and Ocular Vestibular Evoked Myogenic Potentials in Acute Vestibular Neuritis.

OBJECT: Vestibular evoked myogenic potentials (VEMPs) and the subjective visual horizontal (SVH) (or vertical [SVV]) have both been considered tests of otolith function: ocular-VEMPs (oVEMPs) utricular function, cervical VEMPs (cVEMPs) saccular function. Some studies have reported association between decreased oVEMPs and SVH, whereas others have not. DESIGN: A retrospective study of test results. SETTING: A tertiary, neuro-otology clinic, Royal Prince Alfred Hospital, Sydney, Australia. METHOD: We analyzed results in 130 patients with acute vestibular neuritis tested within 5 days of onset. We sought correlations between the SVH, oVEMPs, and cVEMPs to air-conducted (AC) and bone-conducted (BC) stimulation. RESULTS: The SVH deviated to the side of lesion, in 123 of the 130 AVN patients, by 2.5 to 26.7 degrees. Ninety of the AVN patients (70%) had abnormal oVEMPs to AC, BC or both stimuli, on the AVN side (mean asymmetry ratio ± SD [SE]): (64 ± 45.0% [3.9]). Forty-three of the patients (35%) had impaired cVEMPs to AC, BC or both stimuli, on the AVN side, [22 ± 41.6% (4.1)]. The 90 patients with abnormal oVEMP values also had abnormal SVH. Correlations revealed a significant relationship between SVH offset and oVEMP asymmetry (r = 0.80, p < 0.001) and a weaker relationship between SVH offset and cVEMP asymmetry (r = 0.56, p < 0.001). CONCLUSIONS: These results indicate that after an acute unilateral vestibular lesion, before there has been a chance for vestibular compensation to occur, there is a significant correlation between the SVH, and oVEMP results. The relationship between SVH offset and oVEMP amplitude suggests that both tests measure utricular function.

Ocular and cervical vestibular evoked myogenic potentials to 500 Hz fz bone-conducted vibration in superior semicircular canal dehiscence.

OBJECTIVE: The aim of this study was to investigate the effect of superior semicircular canal dehiscence (SSCD) on the n10 component of the ocular vestibular evoked myogenic potential (oVEMP n10) and the p13-n23 component of the cervical vestibular evoked myogenic potential (cVEMP p13-n23) evoked by 500 Hz bone-conducted vibration (BCV) at the midline forehead at the hairline (Fz) in 26 patients with computed tomography-verified SSCD. Previous evidence has led to the proposal that the oVEMP n10 is of utricular origin whereas the cVEMP p13-n23 is of saccular origin. The question is can the oVEMP n10 to 500 Hz BCV indicate SSCD? DESIGN: A hand-held Bruel & Kjaer 4810 Minishaker was used to provide BCV stimulation using surface electromyography electrodes to record oVEMP n10 and cVEMP p13-n23. The stimulus was 7 msec bursts of 500 Hz BCV at either Fz or at the vertex of the skull (Cz). Twenty-seven healthy subjects were tested in the same paradigm. RESULTS: In response to 500 Hz Fz BCV in SSCD patients the oVEMP n10 amplitude beneath the contraSSCD eye was substantially and significantly larger than the oVEMP n10 beneath the ipsiSSCD eye, whereas in these same patients the cVEMP p13-n23 amplitude over the ipsiSSCD sternocleidomastoid muscle to Fz BCV was slightly but significantly larger than the cVEMP p13-n23 amplitude over the contraSSCD sternocleidomastoid muscle. In SSCD patients there was a significant relationship between the size of the dehiscence and the amplitude of the contralateral oVEMP n10 potential. The oVEMP n10 to Cz stimulation was still present in SSCD patients, but small or absent in healthy subjects. CONCLUSIONS: In response to 500 Hz Fz BCV an asymmetrical oVEMP n10 with a significantly increased amplitude of contralesional oVEMP n10 (compared with population values of healthy subjects) is a simple useful indicator of SSCD, confirmed by the Cz response. oVEMP testing with 500 Hz Fz BCV allows very simple, very fast identification of a probable unilateral SSCD.

Capturing vertigo in the emergency room: three tools to double the rate of diagnosis.

OBJECTIVE: Many patients attending the emergency room (ER) with vertigo, leave without a diagnosis. We assessed whether the three tools could improve ER diagnosis of vertigo. METHODS: A prospective observational study was undertaken on 539 patients presenting to ER with vertigo. We used three tools: a structured-history and examination, nystagmus video-oculography (VOG) in all patients, additional video head-impulse testing (vHIT) for acute-vestibular-syndrome (AVS). RESULTS: In the intervention-group (n = 424), case-history classified AVS in 34.9%, episodic spontaneous-vertigo (ESV 32.1%), and episodic positional-vertigo (EPV 22.6%). In AVS, we employed "Quantitative-HINTS plus" (Head-Impulse, Nystagmus and Test-of-Skew quantified by vHIT and VOG, audiometry) to identify vestibular-neuritis (VN) and stroke (41.2 and 31.1%). vHIT gain ≤ 0.72, catch-up saccade amplitude > 1.4○, saccade-frequency > 154%, and unidirectional horizontal-nystagmus, separated stroke from VN with 93.1% sensitivity and 88.5% specificity. In ESV, 66.2 and 14% were diagnosed with vestibular migraine and Meniere's Disease by using history and audiometry. Horizontal-nystagmus velocity was lower in migraine 0.4 ± 1.6○/s than Meniere's 5.7 ± 5.5○/s (p < 0.01). In EPV, benign positional vertigo (BPV) was identified in 82.3% using VOG. Paroxysmal positional-nystagmus lasting < 60 s separated BPV from non-BPV with 90% sensitivity and 100% specificity. In the control group of ER patients undergoing management-as-usual (n = 115), diagnoses included BPV (38.3%) and non-specific vertigo (41.7%). Unblinded assessors reached a final diagnosis in 90.6 and 30.4% of the intervention and control groups. Blinded assessors provided with the data gathered from each group reached a diagnosis in 86.3 and 41.1%. CONCLUSION: Three tools: a structured-assessment, vHIT and VOG doubled the rate of diagnosis in the ER.

Video-head impulse test in superior canal dehiscence.

BACKGROUND: Superior Canal Dehiscence is classically diagnosed with typical abnormalities on Vestibular Evoked Myogenic Potentials (VEMPs) and Computed Tomography (CT) scans. AIM: This paper discusses the utility of the video Head Impulse Test (vHIT) in SCD. METHODS: Data from 11 ears (8 patients) with SCD were retrospectively reviewed. Results from vHIT, VEMPs and CT and when possible, MRI scans were correlated. An audit of 300 vHIT from patients undergoing routine testing for any neurotological complaint was also conducted to look at the incidence of isolated abnormal superior canal function. RESULTS: 82% of patients (9 ears) with SCD showed abnormal vHIT (reduced gain and catch-up saccades) isolated to the affected superior semicircular canal. CONCLUSION: Correlation of the CT and VEMPs are important in forming a diagnosis of SCD. However, if isolated superior canal vHIT abnormalities are demonstrated, it is suggestive of SCD and such patients should be referred for further investigations.

Head impulse compensatory saccades: Visual dependence is most evident in bilateral vestibular loss.

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 vertical-planes reduced slightly. All head-impulse compensatory saccades have a visual contribution, the magnitude of which depends on the symmetry of vestibular-function and saccade latency: BVL is more profoundly affected by vision than UVD, and second saccades more than first saccades. Saccades after UVD are probably triggered by contralateral vestibular function.

The Video Head Impulse Test.

In 1988, we introduced impulsive testing of semicircular canal (SCC) function measured with scleral search coils and showed that it could accurately and reliably detect impaired function even of a single lateral canal. Later we showed that it was also possible to test individual vertical canal function in peripheral and also in central vestibular disorders and proposed a physiological mechanism for why this might be so. For the next 20 years, between 1988 and 2008, impulsive testing of individual SCC function could only be accurately done by a few aficionados with the time and money to support scleral search-coil systems-an expensive, complicated and cumbersome, semi-invasive technique that never made the transition from the research lab to the dizzy clinic. Then, in 2009 and 2013, we introduced a video method of testing function of each of the six canals individually. Since 2009, the method has been taken up by most dizzy clinics around the world, with now close to 100 refereed articles in PubMed. In many dizzy clinics around the world, video Head Impulse Testing has supplanted caloric testing as the initial and in some cases the final test of choice in patients with suspected vestibular disorders. Here, we consider seven current, interesting, and controversial aspects of video Head Impulse Testing: (1) introduction to the test; (2) the progress from the head impulse protocol (HIMPs) to the new variant-suppression head impulse protocol (SHIMPs); (3) the physiological basis for head impulse testing; (4) practical aspects and potential pitfalls of video head impulse testing; (5) problems of vestibulo-ocular reflex gain calculations; (6) head impulse testing in central vestibular disorders; and (7) to stay right up-to-date-new clinical disease patterns emerging from video head impulse testing. With thanks and appreciation we dedicate this article to our friend, colleague, and mentor, Dr Bernard Cohen of Mount Sinai Medical School, New York, who since his first article 55 years ago on compensatory eye movements induced by vertical SCC stimulation has become one of the giants of the vestibular world.

Vestibular neuritis affects both superior and inferior vestibular nerves.

OBJECTIVE: To characterize the profiles of afferent dysfunction in a cross section of patients with acute vestibular neuritis using tests of otolith and semicircular canal function sensitive to each of the 5 vestibular end organs. METHODS: Forty-three patients fulfilling clinical criteria for acute vestibular neuritis were recruited between 2010 and 2016 and studied within 10 days of symptom onset. Otolith function was evaluated with air-conducted cervical and bone-conducted ocular/vestibular evoked myogenic potentials and the subjective visual horizontal test. Canal-plane video head impulse tests (vHITs) assessed the function of each semicircular canal. Patterns of recovery were investigated in 16 patients retested after a 6- to 12-month follow-up period. RESULTS: Rates of horizontal canal (97.7%), anterior canal (90.7%), and utricular (72.1%) dysfunction were significantly higher than rates of posterior canal (39.5%) and saccular (39.0%) dysfunction (p < 0.008). Twenty-four patients (55.8%) had abnormalities localizing to both vestibular nerve divisions; 18 patients (41.9%) had superior neuritis; and 1 patient (2.3%) had inferior neuritis. A test battery that included horizontal and posterior canal vHIT and the cervical/vestibular evoked myogenic potentials identified superior or inferior neuritis in all patients tested acutely. Eight of 16 patients who were retested at follow-up had recovered a normal vestibular evoked myogenic potential and vHIT profile. CONCLUSIONS: Acute vestibular neuritis most often affects both vestibular nerve divisions. The horizontal vHIT alone identifies superior nerve dysfunction in all patients with vestibular neuritis tested acutely, whereas both cervical/vestibular evoked myogenic potentials and posterior vHIT are necessary for diagnosing inferior vestibular nerve involvement.

Vertigo with sudden hearing loss: audio-vestibular characteristics.

Acute vertigo with sudden sensorineural hearing loss (SSNHL) is a rare clinical emergency. Here, we report the audio-vestibular test profiles of 27 subjects who presented with these symptoms. The vestibular test battery consisted of a three-dimensional video head impulse test (vHIT) of semicircular canal function and recording ocular and cervical vestibular-evoked myogenic potentials (oVEMP, cVEMP) to test otolith dysfunction. Unlike vestibular neuritis, where the horizontal and anterior canals with utricular function are more frequently impaired, 74 % of subjects with vertigo and SSNHL demonstrated impairment of the posterior canal gain (0.45 ± 0.20). Only 41 % showed impairment of the horizontal canal gains (0.78 ± 0.27) and 30 % of the anterior canal gains (0.79 ± 0.26), while 38 % of oVEMPs [asymmetry ratio (AR) = 41.0 ± 41.3 %] and 33 % of cVEMPs (AR = 47.3 ± 41.2 %) were significantly asymmetrical. Twenty-three subjects were diagnosed with labyrinthitis/labyrinthine infarction in the absence of evidence for an underlying pathology. Four subjects had a definitive diagnosis [Ramsay Hunt Syndrome, vestibular schwannoma, anterior inferior cerebellar artery (AICA) infarction, and traction injury]. Ischemia involving the common-cochlear or vestibulo-cochlear branches of the labyrinthine artery could be the simplest explanation for vertigo with SSNHL. Audio-vestibular tests did not provide easy separation between ischaemic and non-ischaemic causes of vertigo with SSNHL.

A new saccadic indicator of peripheral vestibular function based on the video head impulse test.

OBJECTIVE: While compensatory saccades indicate vestibular loss in the conventional head impulse test paradigm (HIMP), in which the participant fixates an earth-fixed target, we investigated a complementary suppression head impulse paradigm (SHIMP), in which the participant is fixating a head-fixed target to elicit anticompensatory saccades as a sign of vestibular function. METHODS: HIMP and SHIMP eye movement responses were measured with the horizontal video head impulse test in patients with unilateral vestibular loss, patients with bilateral vestibular loss, and in healthy controls. RESULTS: Vestibulo-ocular reflex gains showed close correlation (R(2) = 0.97) with slightly lower SHIMP than HIMP gains (mean gain difference 0.06 ± 0.05 SD, p < 0.001). However, the 2 paradigms produced complementary catch-up saccade patterns: HIMP elicited compensatory saccades in patients but rarely in controls, whereas SHIMP elicited large anticompensatory saccades in controls, but smaller or no saccades in bilateral vestibular loss. Unilateral vestibular loss produced covert saccades in HIMP, but later and smaller saccades in SHIMP toward the affected side. Cumulative HIMP and SHIMP saccade amplitude differentiated patients from controls with high sensitivity and specificity. CONCLUSIONS: While compensatory saccades indicate vestibular loss in conventional HIMP, anticompensatory saccades in SHIMP using a head-fixed target indicate vestibular function. SHIMP saccades usually appear later than HIMP saccades, therefore being more salient to the naked eye and facilitating vestibulo-ocular reflex gain measurements. The new paradigm is intuitive and easy to explain to patients, and the SHIMP results complement those from the standard video head impulse test. CLASSIFICATION OF EVIDENCE: This case-control study provides Class III evidence that SHIMP accurately identifies patients with unilateral or bilateral vestibulopathies.

Benign paroxysmal positional vertigo can interfere with the cardiac response to head-down tilt.

OBJECTIVE: To assess the pulse rate and the respiratory rate responses to head-down tilt of the whole body in the plane of the posterior canals in healthy subjects and in patients with benign paroxysmal positional vertigo (BPPV). BACKGROUND: Although BPPV attacks are usually accompanied by autonomic symptoms, there are no studies assessing autonomic responses during triggering maneuvers for BPPV, neither in healthy subjects nor in patients. METHODS: We evaluated nine healthy subjects and four BPPV patients (3 unilateral and 1 bilateral). Using a two-axis rotator, from an upright position they were rotated 135 degrees backwards to head-down tilt, either in the plane of the right or the left posterior canal. RESULTS: In healthy subjects, head-down tilt always induced a significant decrease of the pulse rate, which was similar after rotation to the right and to the left posterior canals. This response was observed in patients with unilateral BPPV only when they were rotated toward the nonaffected side, and it was not evident when they were rotated toward the affected side (p < 0.025). In the patient with bilateral BPPV, no change of the pulse rate was observed after rotation toward the right or to the left posterior canal. Although, in all the patients, the respiratory rate increased during the tilt, a similar increase was observed in two healthy subjects. CONCLUSION: After rotation in the plane of the affected semicircular canal, BPPV can interfere with the cardiac response to head-down tilt of the whole body.

Horizontal Eye Position Affects Measured Vertical VOR Gain on the Video Head Impulse Test.

BACKGROUND/HYPOTHESIS: With the video head impulse test (vHIT), the vertical VOR gain is defined as (vertical eye velocity/vertical head velocity), but compensatory eye movements to vertical canal stimulation usually have a torsional component. To minimize the contribution of torsion to the eye movement measurement, the horizontal gaze direction should be directed 40° from straight ahead so it is in the plane of the stimulated canal plane pair. HYPOTHESIS: as gaze is systematically moved horizontally away from canal plane alignment, the measured vertical VOR gain should decrease. STUDY DESIGN: Ten healthy subjects, with vHIT measuring vertical eye movement to head impulses in the plane of the left anterior-right posterior (LARP) canal plane, with gaze at one of five horizontal gaze positions [40°(aligned with the LARP plane), 20°, 0°, -20°, -40°]. METHODS: Every head impulse was in the LARP plane. The compensatory eye movement was measured by the vHIT prototype system. The one operator delivered every impulse. RESULTS: The canal stimulus remained identical across trials, but the measured vertical VOR gain decreased as horizontal gaze angle was shifted away from alignment with the LARP canal plane. CONCLUSION: In measuring vertical VOR gain with vHIT the horizontal gaze angle should be aligned with the canal plane under test.

What does the dissociation between the results of video head impulse versus caloric testing reveal about the vestibular dysfunction in Ménière's disease?

CONCLUSION: It is suggested that the different results of rotational (video head impulse - vHIT) and caloric tests in patients with Ménière's disease (MD) may be a consequence of the physical enlargement of the membranous duct in the hydropic labyrinths in MD, causing a reduced response to caloric stimulation. OBJECTIVES: There have been reports that the results of two tests of semicircular canal function, the caloric response and the responses to vHIT do not agree. This retrospective study at a tertiary referral hospital examined this disagreement. METHODS: This study reviewed the data of 22 patients who met the AAO-HNS criteria for MD and who had both caloric and vHIT testing. RESULTS: There was a clear dissociation: patients with MD had a small or absent response to caloric stimulation of their affected ear, whilst their response to vHIT was in the normal range. DISCUSSION: The accepted Gentine model of the mechanism of caloric stimulation could account for this dissociation: the increased diameter of the semicircular duct in hydropic labyrinths resulting in endolymph circulation within the duct itself and so a smaller thermally induced pressure across the cupula. The increased duct diameter will have little effect on responses to rotation.

What does the head impulse test versus caloric dissociation reveal about vestibular dysfunction in Ménière's disease?

In patients with Ménière's disease (MD), caloric testing can show, depending on the stage and activity of the disease, a variety of results. Between attacks, many, or perhaps even most, patients with unilateral early or mild MD have normal caloric tests; late MD can show abnormalities ranging from mild to severe unilateral canal paresis with or without directional preponderance. The explanation of canal paresis in MD is not clear. The most obvious explanation, severe loss of lateral canal hair cells, is not likely to be correct because hair cell loss will not explain the fluctuating canal paresis to caloric stimulation. In contrast, the published evidence is that rotational testing of semicircular canal function in MD patients typically shows little reduction in function and even enhancement of vestibulo-ocular reflex gain, at least in the early stages of the disease. Here, we offer a novel explanation for this dissociation. We propose that hydropic expansion of the lateral canal membranous labyrinth permits convective recirculation within the duct that allows dissipation of the hydrostatic force that would normally cause cupular displacement and nystagmus in the caloric test.

The Video Head Impulse Test (vHIT) of Semicircular Canal Function - Age-Dependent Normative Values of VOR Gain in Healthy Subjects.

BACKGROUND/HYPOTHESIS: The video Head Impulse Test (vHIT) is now widely used to test the function of each of the six semicircular canals individually by measuring the eye rotation response to an abrupt head rotation in the plane of the canal. The main measure of canal adequacy is the ratio of the eye movement response to the head movement stimulus, i.e., the gain of the vestibulo-ocular reflex (VOR). However, there is a need for normative data about how VOR gain is affected by age and also by head velocity, to allow the response of any particular patient to be compared to the responses of healthy subjects in their age range. In this study, we determined for all six semicircular canals, normative values of VOR gain, for each canal across a range of head velocities, for healthy subjects in each decade of life. STUDY DESIGN: The VOR gain was measured for all canals across a range of head velocities for at least 10 healthy subjects in decade age bands: 10-19, 20-29, 30-39, 40-49, 50-59, 60-69, 70-79, 80-89. METHODS: The compensatory eye movement response to a small, unpredictable, abrupt head rotation (head impulse) was measured by the ICS impulse prototype system. The same operator delivered every impulse to every subject. RESULTS: Vestibulo-ocular reflex gain decreased at high head velocities, but was largely unaffected by age into the 80- to 89-year age group. There were some small but systematic differences between the two directions of head rotation, which appear to be largely due to the fact that in this study only the right eye was measured. The results are considered in relation to recent evidence about the effect of age on VOR performance. CONCLUSION: These normative values allow the results of any particular patient to be compared to the values of healthy people in their age range and so allow, for example, detection of whether a patient has a bilateral vestibular loss. VOR gain, as measured directly by the eye movement response to head rotation, seems largely unaffected by aging.

Superior semicircular canal dehiscence simulating otosclerosis.

This is a report of a patient with an air-bone gap, thought 10 years ago to be a conductive hearing loss due to otosclerosis and treated with a stapedectomy. It now transpires that the patient actually had a conductive hearing gain due to superior semicircular canal dehiscence. In retrospect for as long as he could remember the patient had experienced cochlear hypersensitivity to bone-conducted sounds so that he could hear his own heart beat and joints move, as well as a tuning fork placed at his ankle. He also had vestibular hypersensitivity to air-conducted sounds with sound-induced eye movements (Tullio phenomenon), pressure-induced nystagmus and low-threshold, high-amplitude vestibular-evoked myogenic potentials. Furthermore some of his acoustic reflexes were preserved even after stapedectomy and two revisions. This case shows that if acoustic reflexes are preserved in a patient with an air-bone gap then the patient needs to be checked for sound- and pressure-induced nystagmus and needs to have vestibular-evoked myogenic potential testing. If there is sound- or pressure-induced nystagmus and if the vestibular-evoked myogenic potentials are also preserved, the problem is most likely in the floor of the middle fossa and not in the middle ear, and the patient needs a high-resolution spiral computed tomography (CT) of the temporal bones to show this.