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The uptake of new interface technologies, such as the Oculus Rift have generated renewed interest in virtual reality especially for private entertainment use. However, long standing issues with unwanted side effects, such as nausea from cybersickness, continue to impact on the general use of devices such as head mounted displays. This in turn has slowed the uptake of more immersive interfaces for computer gaming and indeed more serious applications in training and health. In this paper we report a systematic review in the area of cybersickness with a focus on measuring the diverse symptoms experienced. Indeed the related conditions of simulator sickness and motion sickness have previously been well studied and yet many of the issues are unresolved. Here we report on these issues along with a number of measures, both subjective and objective in nature, using either questionnaires or psychophysiological measures that have been used to study cybersickness. We also report on the factors, individual, device related and task dependent that impact on the condition. We conclude that there remains a need to develop more cost-effective and objective physiological measures of both the impact of cybersickness and a person's susceptibility to the condition.

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Psychological resilience can be defined as individual's ability to withstand and adapt to adverse and traumatic events. Resilience is traditionally assessed by subjective reports, a method that is susceptible to self-report bias. An ideal solution to this challenge is the introduction of standardised and validated physiological and/or biological predictors of resilience. We provide a summary of the major concepts in the field of resilience followed by a detailed critical review of the literature around physiological, neurochemical and immune markers of resilience. We conclude that in future experimental protocols, biological markers of resilience should be assesses both during baseline and during laboratory stressors. In the former case the most promising candidates are represented by heart rate variability and by in vitro immune cells assay; in the latter case-by startle responses (especially their habituation) during stress challenge and by cardiovascular recovery after stress, and by cortisol, DHEA and cytokine responses. Importantly, they should be used in combination to enhance predictive power.

Our aim was to expand knowledge of cybersickness - a subtype of motion sickness provoked by immersion into a moving computer-generated virtual reality. Fourteen healthy subjects experienced a 15-min rollercoaster ride presented via a head-mounted display (Oculus Rift), for 3 consecutive days. Heart rate, respiration, finger and forehead skin conductance were measured during the experiment; this was complemented by a subjective nausea rating during the ride and by Motion Sickness Assessment Questionnaire before, immediately after and then 1, 2 and 3h post-ride. Physiological measurements were analysed in three dimensions: ride time, association with subjective nausea rating and experimental day. Forehead, and to a lesser extent finger phasic skin conductance activity showed a correlation with the reported nausea ratings, while alteration in other measured parameters were mostly related to autonomic arousal during the virtual ride onset. A significant habituation was observed in subjective symptom scores and in the duration of tolerated provocation. The latter increased from 7.0±1.3min on the first day to 12.0±2.5min on the third day (p<0.05); this was associated with a reduced slope of nausea rise from 1.3±0.3units/min on the first to 0.7±0.1units/min on the third day (p<0.01). Furthermore, habituation with repetitive exposure was also determined in the total symptom score post-ride: it fell from 1.6±0.1 on the first day to 1.2±0.1 on the third (p<0.001). We conclude that phasic changes of skin conductance on the forehead could be used to objectively quantify nausea; and that repetitive exposure to provocative VR content results in habituation.

Evidence from studies of provocative motion indicates that motion sickness is tightly linked to the disturbances of thermoregulation. The major aim of the current study was to determine whether provocative visual stimuli (immersion into the virtual reality simulating rides on a rollercoaster) affect skin temperature that reflects thermoregulatory cutaneous responses, and to test whether such stimuli alter cognitive functions. In 26 healthy young volunteers wearing head-mounted display (Oculus Rift), simulated rides consistently provoked vection and nausea, with a significant difference between the two versions of simulation software (Parrot Coaster and Helix). Basal finger temperature had bimodal distribution, with low-temperature group (n=8) having values of 23-29 °C, and high-temperature group (n=18) having values of 32-36 °C. Effects of cybersickness on finger temperature depended on the basal level of this variable: in subjects from former group it raised by 3-4 °C, while in most subjects from the latter group it either did not change or transiently reduced by 1.5-2 °C. There was no correlation between the magnitude of changes in the finger temperature and nausea score at the end of simulated ride. Provocative visual stimulation caused prolongation of simple reaction time by 20-50 ms; this increase closely correlated with the subjective rating of nausea. Lastly, in subjects who experienced pronounced nausea, heart rate was elevated. We conclude that cybersickness is associated with changes in cutaneous thermoregulatory vascular tone; this further supports the idea of a tight link between motion sickness and thermoregulation. Cybersickness-induced prolongation of reaction time raises obvious concerns regarding the safety of this technology.

We provoked cybersickness in participants by immersing them in one of two virtual roller coaster rides using a head-mounted display. As simulation technology is often used in training, our main intention was to examine the effect of the experience on their cognitive function. Participant reaction times before and after the experience were measured by averaging their response time to a visual stimulus over a number of trials. We measured a significant reduction in response time before and after the virtual experience. We also examined the changing state of nausea experienced by participants using some simple nausea measures. These included a repeated nausea rating recorded by participants at two-minute intervals. At the completion of the experience, we averaged these ratings to create a standard nausea score. As participants could decide to stop the experience at any time, we also recorded the voluntary duration of the experience. We correlated our measures with two traditional simulator sickness measures, namely the Motion Sickness Susceptibility Questionnaire (MSSQ) and Motion Sickness Assessment Questionnaire (MSAQ). The standard nausea score provided a simple measure of nausea that could be collected at regular intervals with minimal interference to the immersive experience, and was significantly correlated with both the MSSQ and MSAQ scores.

vated QT interval variability is a predictor of malignant ventricular arrhythmia, but the underlying mechanisms are incompletely understood. A recent study in dogs with pacing-induced heart failure suggests that QT variability is linked to cardiac sympathetic nerve activity. The aim of this study was to determine whether increased cardiac sympathetic activity is associated with increased beat-to-beat QT interval variability in patients with essential hypertension. We recorded resting norepinephrine (NE) spillover into the coronary sinus and single-lead, short-term, high-resolution, body-surface ECG in 23 patients with essential hypertension and 9 normotensive control subjects. To assess beat-to-beat QT interval variability, we calculated the overall QT variability (QTVN) as well as the QT variability index (QTVi). Cardiac NE spillover (12.2 Ϯ 6.5 vs. 20.7 Ϯ 14.7, P ϭ 0.03) and QTVi (Ϫ1.75 Ϯ 0.36 vs. Ϫ1.42 Ϯ 0.50, P ϭ 0.05) were significantly increased in hypertensive patients compared with normotensive subjects. QTVN was significantly correlated with cardiac NE spillover (r 2 ϭ 0.31, P ϭ 0.001), with RR variability (r 2 ϭ 0.20, P ϭ 0.008), and with systolic blood pressure (r 2 ϭ 0.16, P ϭ 0.02). Linear regression analysis identified the former two as independent predictors of QTVN. In conclusion, elevated repolarization lability is directly associated with sympathetic cardiac activation in patients with essential hypertension. norepinephrine spillover THE QT INTERVAL OF THE BODY surface ECG reflects global depolarization and repolarization in the ventricular myocardium and undergoes subtle beat-to-beat fluctuations (9). Elevated beat-to-beat QT interval variability has been demonstrated in various cardiac (6, 26) but also noncardiac conditions (4, 36). Importantly, QT variability has been shown to be elevated in dogs before pharmacologically induced Torsades de Pointes (32, 34) and in patients with structural heart disease before ventricular tachycardia/ventricular fibrillation events (33). Furthermore, QT variability was associated with an increased risk of ventricular tachycardia/ventricular fibrillation in patients enrolled in the Multicenter Automatic Defibrillator Implantation Trial (MADIT) II (17) and was predictive of sudden cardiac death in patients with asymptomatic chronic heart failure with mild to moderate left ventricular (LV) diastolic dysfunction (27). However, the mechanisms contributing to beat-to-beat QT interval variability are incompletely understood. Besides electrical restitution, which reflects the intrinsic adaptation of the action potential duration to changes in cycle length (14), the autonomic nervous system is thought to play a key role in the genesis of beat-to-beat QT interval variability. Previous studies addressing this issue have provided conflicting results. A recent study in dogs showed that QT variability was related to left stellate-ganglion activity, but only after the dogs had developed heart failure (28). In healthy humans, pharmacological activation or blockade of ␤-adren...