Increasing levels of vehicle automation are envisioned to allow drivers to engage in other activities but are also likely to increase the incidence of Carsickness or Motion Sickness (MS). Ideally, MS is studied in a safe and controlled environment, such as a driving simulator. However, only few studies address the suitability of driving simulators to assess MS. In this study, we validate a moving base driving simulator for MS research by comparing the symptoms and time course of MS between a real-road driving scenario and a rendition of this scenario in a driving simulator, using a within-subjects design. 25 participants took part as passengers in an experiment with alternating sections (slaloming, stop-and-go) with normal and provocative driving styles. Participants performed Sudoku puzzles (eyes-off-road) during both scenarios and reported MIsery SCale (MISC) scores at 30 s intervals. Motion Sickness Assessment Questionnaire (MSAQ) scores were collected upon completion of either scenario. Overall, the results indicate that MS was more severe in the car than in the simulator. Nevertheless, significant correlations were found between individual MS in the car and simulator for 3 out of 4 MSAQ symptom categories (0.48 < r < 0.73, p < 0.02), with a strong overall correlation (r = 0.57, p = 0.004). MS onset times were similar between the car and the simulator, and sickness fluctuations as a result of driving style showed a similar pattern between scenarios, albeit more pronounced in the car. Based on observed similarities in MS, we conclude these simulator results to have relative validity. We attribute the observed reduction of MS severity in the simulator to the downscaling of the motion by the Motion Cueing Algorithm (MCA). These results suggest that, at least in eyes-off-road conditions, findings on MS from simulator studies may generalize to real vehicles after application of a conversion factor. This conversion factor is likely to depend on simulator and MCA characteristics.

Driving simulators are an increasingly important tool to develop vehicle functionalities and to study driver or passenger responses. A major hindrance to the use and validity of such studies is Simulator Sickness (SS). Several studies have suggested a positive relation between improvements in simulator fidelity and the likelihood of sickness. We hypothesized that this relation only holds true for static (fixed-base) simulators, and that increased fidelity in fact reduces simulator sickness in dynamic (moving-base) simulators. We performed a meta-analysis investigating the relation between sickness and fidelity in static and dynamic systems. A literature search yielded a total of 41 simulator studies that varied aspects of mechanical and/or visual fidelity and assessed SS for the same driving conditions and the same or equivalent participant groups. Evaluation of a model synthesizing the findings of these studies indicates that SS decreases with visual fidelity, and suggests that this effect may be negated for static simulators. The results of the modeling efforts thereby provide some support for the hypothesis that increased fidelity can reduce SS in dynamic simulators. Based on the evaluation of the literature we also note particular shortcomings and gaps in available research. Finally, we make recommendations for specific experiments that may fill these gaps and allow definitive conclusions on the role of simulator fidelity in SS.

Motion sickness is a nearly universal response to the unnatural motions that are experienced when traveling by means other than the body’s own faculties; in artificial realities; and in micro- and partial gravity environments. Despite being a known malady since ancient times, its underlying mechanisms, as well as the marked interpersonal variability in susceptibility, remain incompletely understood. While efferent brain-to-body signaling pathways involved in motion sickness have been previously described, recent findings on the functional role of the gut’s (neuro)epithelial cells and microbiome point to a more intricate biological control system than previously appreciated. We examine (afferent) anatomical, hormonal, immune, and extracellular brain-body pathways, and their potential role in motion sickness etiology. This perspective proposes that an additional route may contribute to the pathophysiology of motion sickness, potentially under regulatory influence of the enteric nervous system. Candidate initiators, acting on these pathways, include humoral agents, enteroendocrine cells, and the gut microbiome.