Ethanol-Induced Vestibular Dysfunction as a Model for Bilateral Vestibular Syndrome: Similarities in Video Head...

The goal of this study was to compare video head impulse test, video-oculography, and clinical balance test changes induced by ethanol consumption, in order to acquire a model for acute bilateral vestibular syndrome.

Four healthy adult men and 5 healthy adult women were recruited as volunteers in the study. Initial video head impulse test, videooculography, and clinical balance test examinations were made. Participants proceeded to drink standard alcohol doses until a maximum of 1.2‰ breath alcohol concentration was reached. Video head impulse test and clinical balance tests were repeated at every 0.2‰ breath alcohol concentration interval and at the final 1.0-1.2‰ breath alcohol concentration range. Video-oculography examinations were repeated at 1.0- 1.2‰ breath alcohol concentration.

Decrease in mean vestibulo-ocular gain at 60 ms between the 0‰ and 1.0-1.2‰ was 0.16 on the left side (P < .05) and 0.16 on the right side (P < .05). A borderline abnormality (mean 0.79/0.82) (left/right) was observed in vestibulo-ocular gain at the highest breath alcohol concentration. Corrective saccades increased significantly in amplitude and latency. There was a statistically significant, symmetrical decrease in video-oculography smooth pursuit gain. Saccade latency increased but statistically significantly only with right-sided cycles. Saccade accuracy remained constant. Optokinetic reflex gain showed significant decrease. Romberg's test was performed with normal results initially and at 1.0-1- 2‰ breath alcohol concentration.

Ethanol produces a symmetrical loss in vestibulo-ocular gain measured by video head impulse test. Ethanol also decreases smooth eye pursuit gain and increases pro-saccade latency. Similar findings can be made in vestibular disorders as well as in cerebellar dysfunction. Central pathology should be ruled out in acute bilateral vestibular syndrome.