Abstract
Extended reality (XR) environments, such as simulators, augmented reality, and virtual reality are major techniques in contemporary AI and entertainment systems. Cybersickness (CS) is a motion-sickness experienced by many users of XR. CS causes debilitating nausea, disorientation, and oculomotor issues. Treatment and prevention for motion-sickness typically involves drugs with sedative properties that impair task performance. These drugs are non-specific to CS and counter intuitive for enabling activity within XR. Our paper finds that there are specific spatiotemporal patterns of brain activity in certain functional networks related to CS and offers a method for the analysis of these patterns. The method can predict CS ahead of its onset and most importantly it suggests what intervention to apply in order to prevent CS in individuals. We apply a novel approach to CS prevention by using our previously developed spiking neural network (SNN) method, which can predict CS using electroencephalogram (EEG) pre-VR usage, before applying neuromodulation to disrupt CS-related functional networks in the brain. This approach provides an additional layer of screening before intervention with high-definition transcranial direct current stimulation (HD-tDCS). The study recruited healthy CS susceptible participants (9 male, 10 female, n = 19, 18–36 years old) and used a within-subjects design. EEG (32-channel, 10–10-configuration) was monitored at seated-rest and processed through the SNN for CS prediction. Immediately following a positive prediction, either sham, anodal or cathodal HD-tDCS was applied at the Cz area (5-min, 1.5 mA, 30 s-ramp-up/down) with subsequent 10-min VR immersion to record CS events. Main results: Cathodal stimulation yielded a significantly higher number of successful preventions compared to anodal (*p = 0.01) and sham (***p = 0.00056), achieving a large effect size (> 0.8) with a 47% reduction in CS likelihood. Significance: The treatment was hypothesized to work through disruption of activity at the motor processing and planning regions under Cz. The area appears to be a marker of ongoing CS susceptibility, and also a contributor towards the condition.