Gentamicin vestibulotoxicity with modern systemic dosing regimens: a prospective study using video-oculography.

Objectives: To determine the incidence of gentamicin vestibulotoxicity with current dosing regimens, and to evaluate the feasibility of routine video-oculography on all patients given gentamicin. Materials and methods: In this prospective incidence study serial horizontal vestibulo-ocular reflex (HVOR) gain measurements were recorded using video-oculography on adult inpatients receiving intravenous gentamicin. The primary outcome was the proportion of patients developing impairment of their HVOR gain. Results: After exclusions, 42 patients were included in the analysis. Three patients (7.1%) developed asymptomatic vestibulotoxicity, exact 95% confidence interval 1.5-19.5%. In two of these patients the deficit resolved within several hours. No patients developed symptomatic vestibulotoxicity. There was no evidence for a generalised reduction in group HVOR gain with time. HVOR gain was not associated with total gentamicin dose, dynamic visual acuity or subjective imbalance. Conclusions and significance: Gentamicin may cause reversible, asymptomatic vestibulotoxicity. Video-oculography may be useful to monitor for vestibulotoxicity in patients treated with gentamcin; however, testing all patients routinely may be challenging.

Comparison of the video head impulse test with the caloric test in patients with sub-acute and chronic vestibular disorders.

The aim of this prospective register-based study was to compare video Head Impulse Tests (vHIT) with caloric tests on 173 patients assessed by a tertiary Neurology referral centre who had been referred for investigation of dizziness or vertigo and whose symptom duration was one month or longer. Abnormal vHIT was defined as angular velocity gain (peak eye velocity/peak head velocity) less than 0.79 at 80 ms and 0.75 at 60 ms, which was two standard deviations below our institutions' lower limit of normal; together with refixation saccades. Abnormal bi-thermal caloric testing defined unilateral hypofunction as a 25% difference using Jongkee's formula and bilateral hypofunction was defined by the sum of the peak slow phase velocities over the four irrigations being <20°/s. Sixty patients had abnormal results on one or both tests, of whom 51 had unilateral and nine bilateral hypofunction. With caloric testing considered as the gold standard, the sensitivity (95% CI) of the vHIT was 18/52, 34.6% (22.0-49.1), and the specificity (95% CI) was 113/121, 93.4% (87.4-97.1). However vHIT was more sensitive in the nine patients with bilateral hypofunction with 100% abnormal vHIT results while only 4/9, 44% had abnormal caloric results. In conclusion these results support the continued use of both vHIT and caloric tests in patients with sub-acute and chronic vestibular symptoms, especially if the vHIT is normal.

Age dependent normal horizontal VOR gain of head impulse test as measured with video-oculography.

BACKGROUND: The head impulse test (HIT) is a recognised clinical sign of the high frequency vestibulo-ocular reflex (VOR), which can be quantified with video-oculography. This measures the VOR gain as the ratio of angular eye velocity to angular head velocity. Although normative data is available for VOR gain with video-oculography, most normal studies in general include small numbers of subjects and do not include analysis of variation of VOR gain with age. The purpose of our study was to establish normative data across 60 control subjects aged 20 to 80 years to represent a population distribution. METHODS: Sixty control subjects without any current or previous form of brain disorder or vertigo participated in this study and form the basis for future comparison to patients with vestibular lesions. The relationship between the horizontal vestibulo-ocular reflex (HVOR) velocity gain and age was analysed using a mixed regression model with a random effect for subjects. Differences in testing technique were assessed to ensure reliability in results. RESULTS: The mean HVOR velocity gain of 60 normal subjects was 0.97 (SD = 0.09) at 80 ms and 0.94 (SD = 0.10) at 60 ms. The 2 SD lower limit of normal HVOR velocity gain was 0.79 at 80 ms and 0.75 at 60 ms. No HVOR velocity gain fell below 0.76 and 0.65 at 80 ms and 60 ms respectively. The HVOR velocity gain declined by 0.012 and 0.017 per decade as age increased at 80 ms and 60 ms respectively. A non-physiologically high horizontal HVOR velocity gain was found to occur in tests where passive HITs were predictable in direction and time and where target distance was below 0.70 m. CONCLUSIONS: Normative data with respect to HVOR velocity gain decreases slightly with age, but with careful attention to methodology the 2 SD lower limit of normal is relatively robust across a wide age range and into the eighth decade, without requirement for adjustment with age.