A computational model of motion sickness dynamics during passive self-motion in the dark.

Predicting the time course of motion sickness symptoms enables the evaluation of provocative stimuli and the development of countermeasures for reducing symptom severity. In pursuit of this goal, we present an Observer-driven model of motion sickness for passive motions in the dark. Constructed in two stages, this model predicts motion sickness symptoms by bridging sensory conflict (i.e., differences between actual and expected sensory signals) arising from the Observer model of spatial orientation perception (stage 1) to Oman's model of motion sickness symptom dynamics (stage 2; presented in 1982 and 1990) through a proposed "Normalized Innovation Squared" statistic. The model outputs the expected temporal development of human motion sickness symptom magnitudes (mapped to the Misery Scale) at a population level, due to arbitrary, 6-degree-of-freedom, self-motion stimuli. We trained model parameters using individual subject responses collected during fore-aft translations and off-vertical axis of rotation motions. Improving on prior efforts, we only used datasets with experimental conditions congruent with the perceptual stage (i.e., adequately provided passive motions without visual cues) to inform the model. We assessed model performance by predicting an unseen validation dataset, producing a Q2 value of 0.91. Demonstrating this model's broad applicability, we formulate predictions for a host of stimuli, including translations, earth-vertical rotations, and altered gravity, and we provide our implementation for other users. Finally, to guide future research efforts, we suggest how to rigorously advance this model (e.g., incorporating visual cues, active motion, responses to motion of different frequency, etc.).

Effects of passenger body movements in a visual task during and after vehicle rotation on post-rotatory illusion and motion sickness.

We explored how body movements influence illusory body motion intensity and their association with motion sickness. Twelve individuals who were seated in the back of a passenger car, performed a visual task and were subjected to continuous rotations followed by driving in a straight line. The body movements during and immediately after rotation were categorized as follows: (A) upright posture; (B) leaning the body in the yaw direction towards the rotation center, returning the yaw angle to zero upon transitioning to straight line travel, and tilting in the roll condition and gradually returning to upright; and (C) tilting in roll conditions towards the centripetal direction during rotation and becoming upright upon transitioning to straight line travel. In experiment-1, after spanning half a lap, participants reported the intensity of the illusory motion experienced during straight line travel immediately after rotation. In experiment-2, after travelling up to eight laps, the participants reported the symptom level of motion sickness experienced during two straight sections per lap using the MIsery SCale (MISC). Experiment-1 revealed that condition (C) had significantly larger illusions than Conditions (A) and (B). Experiment-2 revealed that motion sickness progressed significantly more in Condition (C) than in Condition (A). A significant positive correlation was found between the observed MISC and the illusion strength. Our findings suggest that body movements during and immediately after continuous rotation have a significant impact on the illusion strength. Additionally, illusory motion could serve as an indicator of impending motion sickness.

Visual vertigo and motion sickness is different between persistent postural-perceptual dizziness and vestibular migraine.

INTRODUCTION: Persistent postural-perceptual dizziness (PPPD) and vestibular migraine (VM) share symptoms of visual vertigo and motion sickness that can be confusing for clinicians to distinguish. We compare the severity of these symptoms and dynamic subjective visual vertical (dSVV) in these two common vestibular conditions. METHOD: Twenty-nine patients with PPPD, 37 with VM, and 29 controls were surveyed for subjective symptoms using the visual vertigo analogue scale (VVAS) and motion sickness susceptibility questionnaire during childhood (MSA) and the past 10 years (MSB). dSVV is a measure of visual dependence measures perception of verticality against a rotating background (5 deg./s). RESULTS: VVAS revealed contextual differences for dizziness between those with PPPD and VM. Ratings of visual vertigo were most severe in PPPD, less in VM, and mild in controls (VVAS PPPD 27.1, VM 11.2, control 4.6, p < 0.001). MSA was more severe in VM than in PPPD or control (12.8 vs 7.6 vs 8.5, p = 0.01). MSB was more severe in VM than controls (MSB score 12.9 VS 8.1 p = 0.009) but was not different than PPPD (MSB score 10.0, p = 0.10). dSVV alignment was similar among the three groups (p = 0.83). Both VM and PPPD groups had greater simulator sickness than controls after completing the dSVV. CONCLUSIONS: Patients with PPPD report more visual vertigo than those with VM, but a history of motion sickness as a child is more common in VM. Additionally, the environmental context that induces visual vertigo is different between PPPD and VM.

Classification of Visually Induced Motion Sickness Based on Phase-Locked Value Functional Connectivity Matrix and CNN-LSTM.

To effectively detect motion sickness induced by virtual reality environments, we developed a classification model specifically designed for visually induced motion sickness, employing a phase-locked value (PLV) functional connectivity matrix and a CNN-LSTM architecture. This model addresses the shortcomings of traditional machine learning algorithms, particularly their limited capability in handling nonlinear data. We constructed PLV-based functional connectivity matrices and network topology maps across six different frequency bands using EEG data from 25 participants. Our analysis indicated that visually induced motion sickness significantly alters the synchronization patterns in the EEG, especially affecting the frontal and temporal lobes. The functional connectivity matrix served as the input for our CNN-LSTM model, which was used to classify states of visually induced motion sickness. The model demonstrated superior performance over other methods, achieving the highest classification accuracy in the gamma frequency band. Specifically, it reached a maximum average accuracy of 99.56% in binary classification and 86.94% in ternary classification. These results underscore the model's enhanced classification effectiveness and stability, making it a valuable tool for aiding in the diagnosis of motion sickness.

Left parietal involvement in motion sickness susceptibility revealed by multimodal magnetic resonance imaging.

Susceptibility to motion sickness varies greatly across individuals. However, the neural mechanisms underlying this susceptibility remain largely unclear. To address this gap, the current study aimed to identify the neural correlates of motion sickness susceptibility using multimodal MRI. First, we compared resting-state functional connectivity between healthy individuals who were highly susceptible to motion sickness (N = 36) and age/sex-matched controls who showed low susceptibility (N = 36). Seed-based analysis revealed between-group differences in functional connectivity of core vestibular regions in the left posterior Sylvian fissure. A data-driven approach using intrinsic connectivity contrast found greater network centrality of the left intraparietal sulcus in high- rather than in low-susceptible individuals. Moreover, exploratory structural connectivity analysis uncovered an association between motion sickness susceptibility and white matter integrity in the left inferior fronto-occipital fasciculus. Taken together, our data indicate left parietal involvement in motion sickness susceptibility.

Thermal infrared imaging based facial temperature in comparison to ear temperature during a real-driving scenario.

Motion Sickness is associated with a variety of symptoms, which differ in occurrence rate and intensity between individuals. In order to research the cause of car sickness and develop countermeasures, it is important to determine symptoms and their severity objectively. A tool for this purpose could be the assessment of physiological reactions due to motion sickness. This paper describes and discusses a methodology to identify changes in facial skin temperatures in a real-driving study. Common techniques had to be adjusted in order to meet the requirements given by the challenges of in-car-recording. The examined data was generated in a previous study, which was designed to research motion sickness in a driving environment. A pre-processing technique had to be developed to magnify features on the face and subsequently improve the tracking in thermal imagery. After the pre-processing, regions of interest (ROI) were manually marked and tracked in thermal images. The thereby assessed facial skin temperatures were compared to tympanic temperatures. Derived temperatures from the forehead as well as from the 20 hottest pixels within the face indicated a better tracking, while the nose tip was more affected by detection errors. The correlation of the three features with the tympanic temperature showed remarkable differences between a baseline measurement and the actual driving. Less than 10% of the data derived during the driving and up to 30% of the data during the baseline measurement correlated highly. It is concluded that detecting changes in facial skin temperature using thermal infrared imaging in a moving car is challenging and results are hardly comparable to tympanic temperatures. Future research should aim at the different influencing factors of skin and tympanic temperature, while enhancing tracking or detection of ROI could be achieved by reducing the passengers' movements or choosing the target area more carefully.

Velocity storage: its multiple roles.

Our research described in this article was motivated by the puzzling finding of the Skylab M131 experiments: head movements made while rotating that are nauseogenic and disorienting on Earth are innocuous in a weightless, 0-g environment. We describe a series of parabolic flight experiments that directly addressed this puzzle and discovered the gravity-dependent responses to semicircular canal stimulation, consistent with the principles of velocity storage. We describe a line of research that started in a different direction, investigating dynamic balancing, but ended up pointing to the gravity dependence of angular velocity-to-position integration of semicircular canal signals. Together, these lines of research and the theoretical framework of velocity storage provide an answer to at least part of the M131 puzzle. We also describe recently discovered neural circuits by which active, dynamic vestibular, multisensory, and motor signals are interpreted as either appropriate for action and orientation or as conflicts evoking motion sickness and disorientation.

Vestibular modulation of skin sympathetic nerve activity in sopite syndrome induced by low-frequency sinusoidal motion.

Sopite syndrome, centered around the drowsiness, lethargy, and irritability associated with motion sickness, can be induced by exposure to low-frequency motion. It is known that the vestibular apparatus plays an important role in the pathogenesis of motion sickness, which features several autonomic responses, and we have previously documented increased vestibular modulation of skin sympathetic nerve activity (SSNA) and an increase in skin blood flow associated with nausea. Here, we assessed whether imperceptibly slow sinusoidal motion, sufficient to induce sopite syndrome but not nausea, also modulates SSNA and skin blood flow. Participants were seated upright and exposed to a randomized set of sinusoidal linear accelerations, ranging from 0.03 Hz at 0.5 mG to 0.2 Hz at 5 mG, via a motorized platform. At all frequencies vestibular modulation was greater than the cardiac modulation of SSNA, but cardiac modulation and skin blood flow were both significantly lower during the motion than at baseline. We conclude that sopite syndrome is associated with a marked modulation of sympathetic outflow to the skin and cutaneous vasoconstriction.NEW & NOTEWORTHY Little is known about the autonomic consequences of sopite syndrome-the drowsiness that can be induced by low-amplitude cyclic motion. We recorded skin sympathetic nerve activity (SSNA) in seated participants exposed to slow sinusoidal linear acceleration (0.03-0.2 Hz), which preferentially activates hair cells in the utricular part of the otolithic organs, at amplitudes that generated no sensations of motion. At all frequencies, there was a clear vestibular modulation of SSNA and cutaneous vasoconstriction.

Visual Vertigo, Motion Sickness, and Disorientation in Vehicles.

Environmental circumstances that result in ambiguity or conflict with the patterns of sensory stimulation may adversely affect the vestibular system. The effect of this conflict in sensory information may be dizziness, a sense of imbalance, nausea, and motion sickness sometimes even to seemingly minor daily head movement activities. In some, it is not only exposure to motion but also the observation of objects in motion around them such as in supermarket aisles or other places with visual commotion; this can lead to dizziness, nausea, or a feeling of motion sickness that is referred to as visual vertigo. All people with normal vestibular function can be made to experience motion sickness, although individual susceptibility varies widely and is at least partially heritable. Motorists learn to interpret sensory stimuli in the context of the car stabilized by its suspension and guided by steering. A type of motorist's disorientation occurs in some individuals who develop a heightened awareness of perceptions of motion in the automobile that makes them feel as though they may be rolling over on corners and as though they are veering on open highways or in streaming traffic. This article discusses the putative mechanisms, consequences and approach to managing patients with visual vertigo, motion sickness, and motorist's disorientation syndrome in the context of chronic dizziness and motion sensitivity.

Mal de Debarquement Syndrome.

Mal de debarquement syndrome (MdDS) is a disorder of persistent vertigo characterized by a feeling of oscillation such as rocking, bobbing, or swaying. It is triggered by passive motion, typically by exposure to water, air, or land transportation. This syndrome affects middle-aged individuals who are predominantly women. MdDS presents as a balance disorder that carries significant risk of morbidity due to both the direct effects of balance impairment and associated symptoms of fatigue, cognitive slowing, and visual motion intolerance. The Barany Society will be publishing criteria for diagnosing persistent MdDS. In addition, more insight has been gained into the pathophysiology of MdDS, with current hypotheses pointing to a cerebral and cerebellar basis. Treatments have expanded beyond medication trials, and now include the use of noninvasive brain stimulation and readaptation of the vestibulo-ocular reflex.

Reduction of cybersickness during and immediately following noisy galvanic vestibular stimulation.

The mechanism underlying cybersickness during virtual reality (VR) exposure is still poorly understood, although research has highlighted a causal role for visual-vestibular sensory conflict. Recently established methods for reducing cybersickness include galvanic vestibular stimulation (GVS) to mimic absent vestibular cues in VR, or vibration of the vestibular organs to add noise to the sensory modality. Here, we examined if applying noise to the vestibular system using noisy-current GVS affects sickness severity in VR. Participants were exposed to one of the two VR games that were classified as either moderately or intensely nauseogenic. The VR content lasted for 50 min and was broken down into three blocks: 30 min of gameplay during exposure to either noisy GVS (± 1750 µA) or sham stimulation (0 µA), and 10 min of gameplay before and after this block. We characterized the effects of noisy GVS in terms of post-minus-pre-exposure cybersickness scores. In the intense VR condition, we found a main effect of noisy vestibular stimulation on a verbal cybersickness scale, but not for questionnaire measures of cybersickness. Participants reported lower cybersickness scores during and directly after exposure to GVS. However, this difference was quickly extinguished (~ 3-6 min) after further VR exposure, indicating that sensory adaptation did not persist after stimulation was terminated. In contrast, there were no differences between the sham and GVS group for the moderate VR content. The results show the potential for reducing cybersickness with non-invasive sensory stimulation. We address possible mechanisms for the observed effects, including noise-induced sensory re-weighting.

Patients With Vestibular Migraine are More Likely to Have Occipital Headaches than those With Migraine Without Vestibular Symptoms.

OBJECTIVE: To determine whether patients with vestibular migraine are more likely to suffer from an occipital headache than patients with migraine without vestibular symptoms. BACKGROUND: Vestibular migraine is an underdiagnosed disorder in which migraine is associated with vestibular symptoms. Anatomical evidence and symptomatology hint at the involvement of brain structures in the posterior fossa (back of the head location). We hypothesized that vestibular migraine patients are more likely than migraineurs without vestibular symptoms to experience headaches located in the back of the head, that is, occipital headaches. METHODS: A retrospective cross-sectional study was conducted at the University of Iowa Hospital and Clinics. Chart analysis of 169 patients was performed. The primary outcome was the location of the headache in vestibular migraine patients and migraineurs without vestibular symptoms. The secondary outcomes included the association of vestibular migraine with gender, age at onset of headache, age at onset of vestibular symptoms (such as vertigo, head motion-induced dizziness), aura, motion sickness, other associated symptoms, family history of headaches, and family history of motion sickness. RESULTS: In vestibular migraine group, 45/103 (44%) had occipital location for their headaches vs 12/66 (18%) in migraine patients without vestibular symptoms, for an odd's ratio of 3.5 (95% CI = 1.7-7.2, P < .001). Additionally, the age at onset of headache was greater in the vestibular migraine group (28 ± 12 vs 18 ± 9 years, P < .001) and motion sickness was more common (41/98 (42%) in the vestibular migraine group, 1/64 (2%) in the migraine without vestibular symptoms group, P < .001). CONCLUSIONS: This study suggests that patients with vestibular migraine are more likely to have occipital headaches than patients with migraine without vestibular symptoms. Our data support the initiation of a prospective study to determine whether a patient presenting with occipital headaches, with late onset of age of headache, and with a history of motion sickness is at an increased risk for the possible development of vestibular migraine.

Functional brain networks and neuroanatomy underpinning nausea severity can predict nausea susceptibility using machine learning.

KEY POINTS: Nausea is an adverse experience characterised by alterations in autonomic and cerebral function. Susceptibility to nausea is difficult to predict, but machine learning has yet to be applied to this field of study. The severity of nausea that individuals experience is related to the underlying morphology (shape) of the subcortex, namely of the amygdala, caudate and putamen; a functional brain network related to nausea severity was identified, which included the thalamus, cingulate cortices (anterior, mid- and posterior), caudate nucleus and nucleus accumbens. Sympathetic nervous system function and sympathovagal balance, by heart rate variability, was closely related to both this nausea-associated anatomical variation and the functional connectivity network, and machine learning accurately predicted susceptibility or resistance to nausea. These novel anatomical and functional brain biomarkers for nausea severity may permit objective identification of individuals susceptible to nausea, using artificial intelligence/machine learning; brain data may be useful to identify individuals more susceptible to nausea. ABSTRACT: Nausea is a highly individual and variable experience. The central processing of nausea remains poorly understood, although numerous influential factors have been proposed, including brain structure and function, as well as autonomic nervous system (ANS) activity. We investigated the role of these factors in nausea severity and if susceptibility to nausea could be predicted using machine learning. Twenty-eight healthy participants (15 males; mean age 24 years) underwent quantification of resting sympathetic and parasympathetic nervous system activity by heart rate variability. All were exposed to a 10-min motion-sickness video during fMRI. Neuroanatomical shape differences of the subcortex and functional brain networks associated with the severity of nausea were investigated. A machine learning neural network was trained to predict nausea susceptibility, or resistance, using resting ANS data and detected brain features. Increasing nausea scores positively correlated with shape variation of the left amygdala, right caudate and bilateral putamen (corrected P = 0.05). A functional brain network linked to increasing nausea severity was identified implicating the thalamus, anterior, middle and posterior cingulate cortices, caudate nucleus and nucleus accumbens (corrected P = 0.043). Both neuroanatomical differences and the functional nausea-brain network were closely related to sympathetic nervous system activity. Using these data, a machine learning model predicted susceptibility to nausea with an overall accuracy of 82.1%. Nausea severity relates to underlying subcortical morphology and a functional brain network; both measures are potential biomarkers in trials of anti-nausea therapies. The use of machine learning should be further investigated as an objective means to develop models predicting nausea susceptibility.

Motion sickness-susceptible participants exposed to coherent rotating dot patterns show excessive N2 amplitudes and impaired theta-band phase synchronization.

Visually induced motion sickness (VIMS) can occur via prolonged exposure to visual stimulation that generates the illusion of self-motion (vection). Not everyone is susceptible to VIMS and the neural mechanism underlying susceptibility is unclear. This study explored the differences of electroencephalographic (EEG) signatures between VIMS-susceptible and VIMS-resistant groups. Thirty-two-channel EEG data were recorded from 12 VIMS-susceptible and 15 VIMS-resistant university students while they were watching two patterns of moving dots: (1) a coherent rotation pattern (vection-inducing and potentially VIMS-provoking pattern), and (2) a random movement pattern (non-VIMS-provoking control). The VIMS-susceptible group exhibited a significantly larger increase in the parietal N2 response when exposed to the coherent rotating pattern than when exposed to control patterns. In members of the VIMS-resistant group, before vection onset, global connectivity from all other EEG electrodes to the right-temporal-parietal and to the right-central areas increased, whereas after vection onset the global connectivity to the right-frontal area reduced. Such changes were not observed in the susceptible group. Further, the increases in N2 amplitude and the identified phase synchronization index were significantly correlated with individual motion sickness susceptibility. Results suggest that VIMS susceptibility is associated with systematic impairment of dynamic cortical coordination as captured by the phase synchronization of cortical activities. Analyses of dynamic EEG signatures could be a means to unlock the neural mechanism of VIMS.

The neural basis of motion sickness.

Although motion of the head and body has been suspected or known as the provocative cause for the production of motion sickness for centuries, it is only within the last 20 yr that the source of the signal generating motion sickness and its neural basis has been firmly established. Here, we briefly review the source of the conflicts that cause the body to generate the autonomic signs and symptoms that constitute motion sickness and provide a summary of the experimental data that have led to an understanding of how motion sickness is generated and can be controlled. Activity and structures that produce motion sickness include vestibular input through the semicircular canals, the otolith organs, and the velocity storage integrator in the vestibular nuclei. Velocity storage is produced through activity of vestibular-only (VO) neurons under control of neural structures in the nodulus of the vestibulo-cerebellum. Separate groups of nodular neurons sense orientation to gravity, roll/tilt, and translation, which provide strong inhibitory control of the VO neurons. Additionally, there are acetylcholinergic projections from the nodulus to the stomach, which along with other serotonergic inputs from the vestibular nuclei, could induce nausea and vomiting. Major inhibition is produced by the GABAB receptors, which modulate and suppress activity in the velocity storage integrator. Ingestion of the GABAB agonist baclofen causes suppression of motion sickness. Hopefully, a better understanding of the source of sensory conflict will lead to better ways to avoid and treat the autonomic signs and symptoms that constitute the syndrome.

Changes in skin blood flow, respiration and blood pressure in participants reporting motion sickness during sinusoidal galvanic vestibular stimulation.

NEW FINDINGS: What is the central question of the study? We have previously shown that sinusoidal galvanic vestibular stimulation induces greater modulation of skin sympathetic nerve activity, but not muscle sympathetic nerve activity, in participants who report nausea during simulated motion, but the effects on skin blood flow and blood pressure are unknown. What is the main finding and its importance? During vestibular stimulation, nausea was associated with a greater increase in skin blood flow and a progressive reduction in skin sympathetic nerve activity, but no changes in muscle sympathetic nerve activity. This emphasizes the differential changes in sympathetic outflow to different tissues during nausea. ABSTRACT: We tested the hypothesis that galvanic vestibular stimulation, which produces illusions of side-to-side swaying, causes a greater reduction in skin blood flow in participants who report stimulation-induced nausea. A retrospective analysis was performed on data obtained in 30 participants. Bipolar sinusoidal galvanic vestibular stimulation (sGVS) was applied across the mastoid processes (±2 mA, 0.08 Hz) for 21 min. ECG, continuous blood pressure, respiration and skin blood flow were recorded. Muscle sympathetic nerve activity was recorded in 17 participants and skin sympathetic nerve activity in 12. Ten participants reported motion sickness, whereas 20 did not. Both groups showed an initial reduction in skin (finger) blood flow during sGVS, followed by a sustained increase and a subsequent return towards baseline levels throughout the stimulation; the increase was greater in those who experienced nausea. The increase fits with the progressive reduction in skin sympathetic nerve activity observed in the nauseous group. Mean blood pressure was significantly lower in those who experienced nausea and showed a much larger increase at the onset of sGVS, compared with those who did not. Moreover, the respiratory rate was higher at the outset for the subjects who experienced nausea, decreasing progressively during sGVS, whereas respiratory rate remained constant in those who did not experience nausea. Heart rate was more labile in the subjects who experienced nausea, showing a sustained increase towards the end of stimulation. We have shown that several autonomic parameters change during the nausea induced by vestibular stimulation, but a sustained decrease in skin blood flow is not a hallmark of incipient motion sickness.

Motion sickness as metaphor: engaging with diversity in STEM.

Science, technology, engineering, and math (STEM) continue to work to increase the diversity of the fields, yet there are still significant historical and societal hurdles to be overcome before we reach full representation throughout STEM. The concept of science identity has become a point of interest in this process; it has been suggested that development of one's identity as a scientist is critical to persistence in the field. Metaphors that are rooted in bodily experience can provide a starting point to understand abstract concepts, including science identity and how we as STEM educators respond to increasing diversity within our fields. Given the history of STEM being predominantly populated by people who are white and male, disorientation or discomfort with increasing diversity is not unexpected, and many women and people of color report discrimination and marginalization as a part of their experience in STEM. Here I present a neuroscience-based metaphor that can serve as a starting point for understanding some of the potential disorientation or discomfort that we may experience as we engage with the increasing diversity of STEM and acknowledge this experience as a normal but temporary part of the process of growth and development as a field. I encourage the development and use of further discipline-based metaphors to enhance our discussion and understanding of this important work.

Lessons Learned: Gastric Motility Assessment During Driving Simulation.

In the era of technological advances and innovations in transportation technologies, application of driving simulators for the investigation and assessment of the driving process provides a safe and suitable testing environment. Although driving simulators are crucial for further improvements in transportation, it is important to resolve one of their main disadvantages-simulator sickness. Therefore, suitable methods for the assessment of simulator sickness are required. The main aim of this paper was to present a non-invasive method for assessing simulator sickness by recording gastric myoelectrical activity-electrogastrography. Open-source hardware for electrogastrography together with recordings obtained in 13 healthy volunteers is presented, and the main aspects of signal processing for artifact cancellation and feature extraction were discussed. Based on the obtained results, it was concluded that slow-wave electrical gastric activity can be recorded during driving simulation by following adequate recommendations and that proposed features could be beneficial in describing non-ordinary electrogastrography signals.

Effects of Visually Induced Motion Sickness on Emergency Braking Reaction Times in a Driving Simulator.

OBJECTIVE: The study explores associations of visually induced motion sickness (VIMS) with emergency braking reaction times (RTs) in driving simulator studies. It examines the effects over the progression of multiple simulated drives. BACKGROUND: Driving simulator usage has many advantages for RT studies; however, if it induces VIMS, the observed driving behavior might deviate from real-world driving, potentially masking or skewing results. Possible effects of VIMS on RT have long been entertained, but the progression of VIMS across simulated drives has so far not been sufficiently considered. METHOD: Twenty-eight adults completed six drives on 2 days in a fixed-base driving simulator. At five points during each drive, pedestrians entered the road, necessitating emergency braking maneuvers. VIMS severity was assessed every minute using the 20-point Fast Motion Sickness Scale. The progression of VIMS was considered in mixed model analyses. RESULTS: RT predictions were improved by considering VIMS development over time. Here, the relationship of VIMS and RT differed across days and drives. Increases in VIMS symptom severity predicted more prolonged RT after repeated drives on a given day and earlier within each drive. CONCLUSION: The assessment of VIMS in RT studies can be beneficial. In this context, VIMS measurements in close temporal proximity to the behaviors under study are promising and offer insights into VIMS and its consequences, which are not readily obtainable through questionnaires. APPLICATION: Driving simulator-based RT studies should consider cumulative effects of VIMS on performance. Measurement and analysis strategies that consider the time-varying nature of VIMS are recommended.

Emotional and Cognitive Modulation of Cybersickness: The Role of Pain Catastrophizing and Body Awareness.

OBJECTIVE: The goal was to investigate the influence of the tendency to catastrophize somatic symptoms and body awareness on motion-related sickness. BACKGROUND: Influences of emotional and cognitive-evaluative processes on the genesis of motion sickness or cybersickness have rarely been investigated. Brain imaging studies showed activation during cybersickness, resembling the pattern found for pain processing. Two aspects often investigated in this context are pain catastrophizing and body awareness. The present two studies investigated the relationship of motion-related sickness to two tendencies involved in pain processing: pain catastrophizing and body awareness. METHOD: In the first study, 115 participants reported their motion sickness history, pain catastrophizing, and body awareness. In the second study, 40 participants were exposed to a virtual reality and reported their experience of cybersickness as well as their pain catastrophizing and body awareness. RESULTS: Pain catastrophizing was positively correlated to motion sickness history and cybersickness. Body awareness did not show a linear effect on motion sickness history or cybersickness. However, the interaction effect of pain catastrophizing and body awareness was significant in both studies. CONCLUSION: Pain catastrophizing seems to have a detrimental effect on cybersickness symptoms. Body awareness moderated the relationship in the sense that the combination of high pain catastrophizing and low body awareness lead to the highest sickness levels. APPLICATION: Affective and cognitive modulation of cybersickness symptoms should be considered when exposing risk groups to motion-related adverse stimuli.