Bilateral vestibular loss is a rare cause of visual disturbance (oscillopsia) and imbalance. When severe, the most common cause is iatrogenic-gentamicin ototoxicity. Bilateral loss is easily diagnosed at the bedside with the dynamic illegible E test. If this test is omitted, it can easily be misdiagnosed as a cerebellar syndrome. Treatment is largely supportive. Care should be taken to avoid medications that suppress vestibular function, and to encourage activity.

Bilateral vestibular weakness (BVW) is a rare cause of imbalance. Patients with BVW complain of oscillopsia. In approximately half of the patients with BVW, the cause remains undetermined; in the remainder, the most common etiology by far is gentamicin ototoxicity, followed by much rarer entities such as autoimmune inner ear disease, meningitis, bilateral Ménière’s disease, bilateral vestibular neuritis, and bilateral vestibular schwannomas. While a number of bedside tests may raise the suspicion of BVW, the diagnosis should be confirmed by rotatory chair testing. Treatment of BVW is largely supportive. Medications with the unintended effect of vestibular suppression should be avoided.

Objective: To determine if a sound evoked myogenic potential could be obtained from the triceps with the recording and stimulus parameters routinely used to obtain a vestibular evoked myogenic potential (VEMP) from the sternocleidomastoid. Study Design: Prospective study of myogenic potentials recorded from the triceps in healthy subjects. We used a monaural acoustic stimulus and measured the unrectified myogenic potential using surface electromyography electrodes, using response-triggered averaging, on the triceps of 18 subjects. Setting: University-affiliated otoneurology clinic. Patients: Eighteen healthy adult volunteers (11 women and 7 men), age ranging between 27 and 36 years. Main Outcome Measures: Latencies and amplitudes of the first two waves of the evoked response. Results: The P1 latency was 36.83 ± 8.42 ms (range, 26.34-57.99 ms; 95% confidence interval [CI], 33.53-40.14 ms), the N1 latency was 43.74 ± 8.80 ms (range, 34.67-66.32 ms; 95% CI, 40.29-47.19 ms), the P1-N1 interlatency was 6.90 ± 1.23 ms (range, 5.21-9.79 ms; 95% CI, 6.42-7.39 ms), and the P1-N1 interamplitude was 93.23 ± 51.25 μV (range, 16.33-206.62 μV; 95% CI, 73.14-113.32 V). Conclusion: A monaural sound stimulus elicits a robust and reproducible surface myogenic potential in triceps muscles.

Acute vestibular neuropathy (AVN), often referred to as vestibular neuritis, is a cranial neuropathy responsible for a significant proportion of cases of acute vertigo. This study describes the spectrum of lesion patterns in AVN as identified by video head impulse testing (vHIT) which assesses the high frequency vestibulo-ocular reflex function of the semicircular canals, and cervical and ocular vestibular evoked myogenic potentials (VEMPs) which assess otolith function. We used vHIT and VEMPs to assess 35 patients with vestibular neuropathy in the acute stage. Unilateral superior division vestibular nerve involvement was the most common variant (57.1%), followed by unilateral superior and inferior division (28.5%), bilateral superior division (8.5%) and unilateral inferior division (5.7%). We observed a partial inverse correlation between the proportion of afferent fibers from an organelle, and the likelihood that the test of that organelle’s function will be abnormal. vHIT and VEMPs provide more detailed characterization of lesion pattern in AVN than caloric testing. Comparison of lesion patterns from neuro-physiological testing with what is known about the proportional distribution of afferent fibers from the vestibular end-organelles suggests a new, neuro-anatomically based insight regarding susceptibility of these pathways to AVN.