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Effect of Ethanol on Visual‐Vestibular Interactions During Vertical Linear Body Acceleration
Author(s) -
Schmäl Frank,
Thiede Oliver,
Stoll Wolfgang
Publication year - 2003
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1097/01.alc.0000087085.98504.8c
Subject(s) - vestibular system , audiology , fixation (population genetics) , eye movement , linear acceleration , stimulation , visual acuity , oscillopsia , visual disturbance , latency (audio) , smooth pursuit , psychology , medicine , ophthalmology , surgery , physics , acceleration , neuroscience , computer science , population , telecommunications , environmental health , classical mechanics
Background: Ethanol led to disturbed dynamic visual acuity (DVA) during vertical linear acceleration (VLA; amplitude, 5 cm; frequency, 1.2 Hz). The aim of this study was to analyze whether suppression of visual‐oculomotor or vestibular pathway is responsible for the disturbance of DVA. Methods: Twenty volunteers were investigated before and after ethanol consumption (mean breath alcohol concentration, 0.32 mg/liter). Vertical eye movements and linear head acceleration were recorded. Tested stimuli were vestibular (VLA in the dark), visual (smooth pursuit), and combined (VLA plus fixation on an earth‐fixed target) stimulation; visual suppression (VLA plus fixation of a head‐fixed target); static visual acuity; and DVA. Parameters of analysis were gain, sensitivity, eye velocity and amplitude, latency between onset of head acceleration and start of eye movement, correct and wrong answers during static visual acuity and DVA testing, feeling of drunkenness (FOD), and breath alcohol concentration. Results: Both during isolated visual and during combined visual‐vestibular stimulation, alcohol induced a significant latency increase. Furthermore, DVA was disturbed after ethanol consumption. Test subjects with a strong alcohol‐induced disturbance of DVA presented during isolated visual stimulation a significantly higher latency change than volunteers with a minor alcohol‐induced disturbance of DVA. On the basis of the FOD, two groups were formed (one with a slight and one with a strong FOD). The two groups differed significantly concerning the alcohol‐induced latency increase during isolated visual stimulation and the alcohol‐induced disturbance of DVA. Conclusions: Ethanol leads to a disturbance of the visual‐oculomotor system and, thus, even during combined visual‐vestibular stimulation, to a latency increase. This “delay” is responsible for the disturbance of DVA. This alcohol‐induced suppression of the visual‐oculomotor system and the disturbance of DVA show a significantly positive correlation with the subjective FOD.

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