ObjectiveTo facilitate the diagnosis of vestibular disorders by patient-initiated capture of ictal nystagmus.MethodsAdults from an Australian neurology outpatient clinic reporting recurrent vertigo were recruited prospectively and taught to self-record spontaneous and positional nystagmus at home while symptomatic, using miniature video-oculography goggles. Consenting patients with ictal videorecordings and a final unblinded clinical diagnosis of Ménière disease (MD), vestibular migraine (VM), or benign paroxysmal positional vertigo (BPPV) were included.ResultsIctal eye videos of 117 patients were analyzed. Of 43 patients with MD, 40 showed high-velocity spontaneous horizontal nystagmus (median slow-phase velocity [SPV] 39.7°/s; 21 showed horizontal nystagmus reversing direction within 12 hours [24 on separate days]). In 44 of 67 patients with VM, spontaneous horizontal (n = 28, 4.9°/s), upbeating (n = 6, 15.5°/s), or downbeating nystagmus (n = 10, 5.1°/s) was observed; 16 showed positional nystagmus only, and 7 had no nystagmus. Spontaneous horizontal nystagmus with SPV >12.05°/s had a sensitivity and specificity of 95.3% and 82.1% for MD (95% confidence interval [CI] 0.84–0.99, 0.71–0.90). Nystagmus direction change within 12 hours was highly specific (95.7%) for MD (95% CI 0.85–0.99). Spontaneous vertical nystagmus was highly specific (93.0%) for VM (95% CI 0.81–0.99). In the 7 patients with BPPV, spontaneous nystagmus was absent or <3°/s. Lying affected-ear down, patients with BPPV demonstrated paroxysmal positional nystagmus. Median time for peak SPV to halve (T50) was 19.0 seconds. Patients with VM and patients with MD demonstrated persistent positional nystagmus (median T50; 93.1 seconds, 213.2 seconds). T50s <47.3 seconds had a sensitivity and specificity of 100% and 77.8% for BPPV (95% CI 0.54–1.00, 0.64–0.88).ConclusionPatient-initiated vestibular event monitoring is feasible and could facilitate rapid and accurate diagnosis of episodic vestibular disorders.
Direction changing horizontal positional nystagmus can be observed in a variety of central and peripheral vestibular disorders. We tested sixty subjects with horizontal positional nystagmus and vertigo on the Epley Omniax(®) rotator. Monocular video recordings were performed with the right or left ear down, in the supine and prone positions. Nystagmus slow-phase velocity (SPV) was plotted as a function of time. Thirty-one subjects diagnosed with horizontal canalolithiasis had paroxysmal horizontal geotropic nystagmus with the affected ear down (onset 0.8 ± 1 s, range 0-4.9 s, duration 11.7-47.9 s, peak SPV 79 ± 67°/s). The SPV peaked at 5-20 s and declined to 0 by 60 s; at 40 s from onset, the average SPV was 1.8 % of the peak. Nine subjects diagnosed with cupulolithiasis had persistent apogeotropic horizontal nystagmus (onset 0.7 ± 1.4 s, range 0-4.3 s). Peak SPV was 54.2 ± 31.8°/s and 26.6 ± 12.2°/s with unaffected and affected ears down, respectively. At 40 s, the average SPV had decayed to only 81 % (unaffected ear down) and 65 % (affected ear down) of the peak. Twenty subjects were diagnosed with disorders other than benign positional vertigo (BPV) [vestibular migraine (VM), Ménière's Disease, vestibular schwannoma, unilateral or bilateral peripheral vestibular loss]. Subjects with VM (n = 13) had persistent geotropic or apogeotropic horizontal nystagmus. On average, at 40 s from nystagmus onset, the SPV was 61 % of the peak. Two patients with Ménière's Disease had persistent apogeotropic horizontal nystagmus; the peak SPV at 40 s ranged between 28.6 and 49.5 % of the peak. Symptomatic horizontal positional nystagmus can be observed in canalolithiasis, cupulolithiasis and diverse central and peripheral vestibulopathies; its temporal and intensity profile could be helpful in the separation of these entities.
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