Intra-Attack Vestibuloocular Reflex Changes in Ménière's Disease

Abstract

Ménière's attack has been shown to temporarily alter the vestibuloocular reflex (VOR). A patient with unilateral Ménière's disease was serially evaluated with the video Head Impulse Test during single, untreated episodes of acute vertigo. Spontaneous nystagmus activity was concurrently recorded in order to establish the three typical phases of Ménière's attack (irritative, paralytic, and recovery) and correlate them with VOR performance. The onset of attack was associated with a quick change in VOR gain on the side of the affected ear. While a rapidly progressive reduction of the VOR was evident at the paralytic nystagmus phase, in the recovery phase the VOR gain returned to normal and the direction of the previous nystagmus reversed. The membrane rupture potassium intoxication theory provides a good foundation with which to explain these dynamic VOR changes and the observed triphasic direction behavior of the spontaneous nystagmus. We additionally postulated that endolymphatic fluid displacement could have a synergic effect during the earliest phase of attack.

Figure 1

(a) The VOR regression gain values on the y-axis shows evolution of the right affected side (red line) and left side (blue line) during a vertigo attack from the beginning (0 minutes before attack) to the symptomatic end (90 minutes). The small plots show the video Head Impulse Test (vHIT) recordings; the velocity trajectories (°/s) of the eye (dark grey lines) and head (light grey lines) are depicted during right and left impulses. There are short time mismatches between the vHIT records and the VNG records (spontaneous nystagmus), which can be attributed to the changes and calibration of each instrument. On the right HIT, note the saturated profile of the eye velocity curve and the low VOR gain (from 1.01 to 0.31) as well as the grouped, same direction corrective saccades (at 0.71 right gain). Note also that, with the progression of the attack (at 0.39 and 0.31 right gain), the untidy saccadic movements observed on the ocular velocity baseline trace are due to the interference effect at the onset of the fast phase of the spontaneous nystagmus. At the end of the acute stage (about 60 minutes), the horizontal nystagmus changes direction, and the eye velocity curve regains its normal trajectory, although the VOR gain still shows a slight asymmetry. A week later, the gain was normal (1.09 right and 1.1 left), and no corrective saccades or spontaneous nystagmus were recorded. Technical conditions of the vHIT: number of head impulses technically accepted for analysis: from 10 to 25. Head velocity: from 140 to 190 (°/sec). (b) Spontaneous nystagmus. Velocity SPV °/sec on the y-axis is shown with fixation (black line) and without fixation (grey line). At 60 minutes, the nystagmus reversed to the right. ^∗The irritative period was not recorded.