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When studying (the effectiveness of countermeasures to) carsickness in a simulator, it currently remains a question whether results still hold true in a real car. This question not only concerns its practical consequences, but the scientific interest in the underlaying mechanisms as well. By reckoning previous observations and new insights focussing on the differences between simulator and car motion as well their Out-the-Window (OtW) visuals, this paper nuances the assumption that (moving base) simulators can be useful in research on driving comfort in autonomous vehicles. It elaborates on six specific issues: 1) the use of fixed base simulators, 2) motion cueing, 3) linear displacement limitations, 4) display limitations, 5) perceptual scaling of visual and vestibular cues, and 6) physical and visually induced self-tilt. The overall conclusion is that only without OtW artificial visuals and when true car motion can be replicated, it is possible to elicit carsickness in a simulator. If motion is limited by displacement, sickness is most severe at 0.35 Hz. Whenever motion cueing and/or artificial OtW visuals are applied, sickness elicited is better described as simulator sickness, then defined as sickness only occurring during the simulated, but not during the real ride.

This study investigated the role of vection (i.e., a visually induced sense of self-motion), optokinetic nystagmus (OKN), and inadvertent head movements in visually induced motion sickness (VIMS), evoked by yaw rotation of the visual surround. These three elements have all been proposed as contributing factors in VIMS, as they can be linked to different motion sickness theories. However, a full understanding of the role of each factor is still lacking because independent manipulation has proven difficult in the past. We adopted an integrative approach to the problem by obtaining measures of potentially relevant parameters in four experimental conditions and subsequently combining them in a linear mixed regression model. To that end, participants were exposed to visual yaw rotation in four separate sessions. Using a full factorial design, the OKN was manipulated by a fixation target (present/absent), and vection strength by introducing a conflict in the motion direction of the central and peripheral field of view (present/absent). In all conditions, head movements were minimized as much as possible. Measured parameters included vection strength, vection variability, OKN slow phase velocity, OKN frequency, the number of inadvertent head movements, and inadvertent head tilt. Results show that VIMS increases with vection strength, but that this relation varies among participants (R2 = 0.48). Regression parameters for vection variability, head and eye movement parameters were not significant. These results may seem to be in line with the Sensory Conflict theory on motion sickness, but we argue that a more detailed definition of the exact nature of the conflict is required to fully appreciate the relationship between vection and VIMS.

Adaptation to a novel gravitational state involves adaptation of vestibular mediated responses, in particular those mediated by the otolith organs. The present paper investigates whether the orientation of Listing's plane, which is under control of otolith signals, is affected by sustained exposure to hypergravity. Subjects were exposed to four G-loads differing in duration (45 or 90 min) and magnitude (2 or 3G). During centrifugation subjects were in a supine position, directing the gravito-inertial acceleration along the naso-occipetal axis. We determined the orientation of Listing's plane before and after each centrifuge run, with the head erect and tilted in pitch. Head tilt in pitch induced a counter-pitch of Listing's plane, which was found to be less pronounced after centrifugation. In addition, exposure to 3G for 90~min induced a small backward tilt of Listing's plane compared to the pretest orientation (head erect). In order to explain these results a hypothesis is discussed, proposing that the orientation of Listing's plane in the head is governed by a head fixed orientation vector that is modulated by the direction of gravity relative to the head. Sustained centrifugation is proposed to decrease this gravitational modulation, leading to the effects observed. This could reflect a shift towards a more body centered frame of reference.

It has been found that sustained centrifugation on Earth may evoke sickness symptoms that are similar to those of the Space Adaptation Syndrome (SAS). As in SAS, incidence of this 'Sickness Induced by Centrifugation' (SIC) is about 50% and the symptoms are particularly evoked by head movements. By systematically varying the G-load and duration of centrifugation, the current study investigated the characteristics of the gravitational stimulus that is required for SIC to occur. Subjects were exposed to centrifugation at 2 and 3Gx, for a duration of 45 and 90 minutes. A standardized head movement protocol was used to evoke SIC after centrifugation. The results show that in six out of 12 subjects (50%) no serious symptoms were elicited. In the remaining subjects, the effects of the 3G runs exceeded those of the 2G runs, and within each G-level symptom intensity was higher for the 90 min than for the 45 min exposure. An exponential fit on this data showed that the time constant of adaptation to the gravitational stimulus was about 60 minutes. This suggests that short duration exposures (i.e. < 60 min) are not likely to induce serious SIC.

At TNO research is ongoing on neuro-vestibular adaptation to altered G-levels. It is well-known that during the first days in weightlessness 50-80% of all astronauts suffer from the Space Adaptation Syndrome (SAS), which involves space motion sickness, spatial disorientation and motion illusions. After return on Earth the problems re-appear, but now also accompanied by postural imbalance. Standard tests for motion sickness, typically applied in astronaut selection programs, do not correlate with SAS at all. TNO developed a method which effectively simulates SAS on Earth, by exposing astronauts to a hypergravity stimulus of 3G in a human centrifuge for one hour. So far we tested the susceptibility for SIC in 12 astronauts and cosmonauts who also rated their susceptibility for SAS in actual spaceflight. The correlation is 100%, suggesting a common mechanism for any G-level transition, whether it is from 1G to 0G or from 3G to 1G. This paper describes the current status of this research.

Illusory self-motion often provokes motion sickness, which is commonly explained in terms of an inter-sensory conflict that is not in accordance with previous experience. Here we address the influence of cognition in motion sickness and show that such a conflict isnotprovocative when the observer believes that the motion illusion is indeed actually occurring. Illusory self-motion and motion sickness were elicited in healthy human participants who were seated on a stationary rotary chair inside a rotating optokinetic drum. Participants knew that both chair and drum could rotate but were unaware of the actual motion stimulus. Results showed that motion sickness was correlated with the discrepancy between participants’perceivedself-motion and participants’beliefsabout the actual motion. Together with the general motion sickness susceptibility, this discrepancy accounted for 51% of the variance in motion sickness intensity. This finding sheds a new light on the causes of visually induced motion sickness and suggests that it is not governed by an inter-sensory conflict per se, but by beliefs concerning the actual self-motion. This cognitive influence provides a promising tool for the development of new countermeasures.