The effect of oral ethanol consumption on eye movements in healthy volunteers

Abstract

Horizontal and vertical eye movements were recorded and analysed with an infrared photoelectric technique in 12 healthy volunteers under various blood alcohol concentrations (0.0, 0.5, 1.0 g/kg body weight, [% per thousand]). The predictive smooth-pursuit tracking and saccadic eye movements were studied in response to unpredictable target jumps and during scanning of a classical kitchen scene and a traffic scene. Smooth-pursuit eye movement gain value decreased dose-dependently and was compensated by an increased number of catch-up saccades. With increasing blood alcohol concentrations peak velocities of horizontal and vertical visually guided reflexive saccades decreased while their latencies to the target increased. At blood alcohol concentrations of 0.5% per thousand and 1.0% per thousand healthy volunteers showed significantly longer mean fixation durations and a lower total number of exploratory saccades when scanning both the classical kitchen scene and the traffic scene. Surprisingly, in both of these scanning tasks the total fixation duration or the relative number of exploratory saccades increased in those scene sectors in which exciting situations were presented. Additionally, the time interval needed to foveate these exciting areas for the first time increased, probably due to an attention deficit. In conclusion, these findings indicate that alcohol consumption impairs the velocity and initiation of saccadic and smooth-pursuit eye movements, but that subjects can nevertheless still recognize exciting and relevant areas of visual scenes. The significant increase in fixation time, however, does not allow scanning of the entire visual scene during an adequate period of time. Therefore the reduced visual exploration caused by alcohol reflects an impaired sensorimotor processing of active visual perception.

Disrupted Eye Movements in Preperimetric Primary Open-Angle Glaucoma

“…The extent of reduction in saccade velocity observed in preperimetric POAG patients is comparable to that observed under intoxication [39][40][41] or sedation. 42 In fact, the 14.1% reduction in average velocity denoted in POAG patients here is even more prominent than that observed with 0.06% to 0.12% blood alcohol level (9%).…”

Saccade and cognitive impairment associated with kava intoxication

“…The saccadic slowing was characterized by a reduced peak velocity of visually guided saccades, although the latency of visually guided saccades was not affected by kava intoxication nor was their duration. Saccade peak velocity is sensitive to the acute effects of sedating drugs including benzodiazepines, barbiturates, anticonvulsants and alcohol and is considered a valuable indicator of the pharmacological effects mediated by the GABA-benzodiazepine receptor complex (Jürgens et al, 1981;Thurston et al, 1984;Richens et al, 1993;Cowley et al, 1994;Kroboth et al, 1998;Moser et al, 1998). An interaction between kava lactones and GABAergic systems is well established in animal studies that show kava lactones cause alterations to the GABA-benzodiazepine receptor complex through their direct actions on sodium-dependent ion channels (Duffield and Jamieson, 1988;Davies et al, 1992;Jussofie et al, 1994;see Cairney et al, 2002 for review).…”

Blood alcohol concentration at 0.06 and 0.10% causes a complex multifaceted deterioration of body movement control

“…Two 30% alcohol drinks yields about 0.06% BAC in a person of 73kg weight. The falls and poorer postural control is probably related to an interference by ethyl alcohol on the sensory and motor synapses in the CNS, causing difficulty in nerve firing and transmission of nerve impulses (Moser et al, 1998).…”