Does alcohol cancel static vestibular compensation?

Acute alcohol intoxication is accompanied by the otoneurological signs of spinocerebellar and vestibulocerebellar ataxia, positional alcohol nystagmus, and ocular motor abnormalities, such as saccadic pursuit and gaze-evoked nystagmus. Some of these ocular motor disturbances possibly result from a transient alcohol-induced dysfunction of the vestibulocerebellar flocculus loop. On the cellular level, ethanol may alter neural activity by several mechanisms, including direct action on neurotransmitter-gated ion channels that lead, for example, to inhibition of N-methyl-D-aspartate and enhancement of GABA receptors. Incidental reports on patients with centrally compensated unilateral peripheral vestibular failure (UVF) mention reduced tolerance to low doses of alcohol. This suggests that alcohol might cancel an already compensated persisting UVF. Indeed, animal studies on compensated hemilabyrinthectomized cats have supported this assumption by showing that intravenously administered alcohol temporarily caused a recurrence of the initial spontaneous nystagmus (SPN). To determine if alcohol neutralizes central vestibular compensatory mechanisms under static conditions in humans in a similar way, we examined 12 patients (10 men; mean age 59.1 16.5 years; range, 23–74 years) with compensated persisting UVF due to vestibular neuritis that had manifested 3 to 69 months before the study. Only patients with unilateral hyporesponsiveness or unresponsiveness ( 25% according to Jongkees’ vestibular paresis formula) to caloric irrigation of the affected ear participated in the study after giving their informed consent. Eight patients exhibited complete unresponsiveness and four showed hyporesponsiveness. Before alcohol intake, none of the patients showed SPN during video-oculographic recordings with eyes open in the dark. Dynamic vestibular function, as assessed with the head thrust maneuver (Curthoys–Halmagyi), was not tested. In analogy to an earlier study on positional alcohol nystagmus, patients ingested 0.8g alcohol/kg body weight (2.5ml vodka/kg body weight) to reach alcohol blood levels of approximately 0.1%. To evaluate the effects of alcohol on ocular motor, vestibulospinal, and perceptional systems in patients with compensated vestibular neuritis, we performed the following measures before and 30 minutes after alcohol intake: (1) a neurological examination focusing on possible alcohol-induced ocular motor disturbances such as saccadic pursuit and gaze-holding deficit, (2) two-dimensional videooculography in complete darkness (to detect SPN); (3) laser scanning ophthalmoscopy to determine ocular torsion (in degrees); (4) posturography on a foam-padded Kistler platform with the eyes open in darkness to assess total sway path values (in m/min), and (5) adjustments of subjective visual vertical under static and dynamic conditions (in degrees). Compared with the neurological examination before ingestion (which showed normal findings), alcohol caused saccadic horizontal and vertical pursuit in 10 of 12 patients and a horizontal gaze-evoked nystagmus in 8 of 12. Spontaneous nystagmus did not recur in any of the 12 patients after ingesting alcohol. No significant displacements of ocular torsion or subjective visual vertical, neither under static nor under dynamic conditions, were observed (Fig 1). The total sway path during upright stance on the force-measuring platform also did not increase; on the contrary, it even tended to decrease after alcohol intake. Fourier analysis of the anterior/ posterior and lateral body sway exhibited a significantly reduced sway activity in the frequency spectrum 3.5 to 8Hz (p 0.05). This effect of alcohol on body sway might be a result of the dose-related biphasic action of alcohol, which either depresses or stimulates depending on its concentration in the blood; a similar finding was reported in a previous study on body sway patterns in healthy volunteers. All in all, our findings show that contrary to what is generally assumed, alcohol in the chosen doses used here did not cause a decompensation (at the perceptional, ocular motor, or vestibular-spinal levels) under static conditions of a compensated vestibular tone imbalance due to a persisting unilateral loss of vestibular function. On the other hand, we do not yet know if alcohol causes a decompensation of dynamic vestibular function as reflected in responses with the head or body moving.