Motion sickness: more than nausea and vomiting

Abstract

Motion sickness is a complex syndrome that includes many features besides nausea and vomiting. This review describes some of these factors and points out that under normal circumstances, many cases of motion sickness go unrecognized. Motion sickness can occur during exposure to physical motion, visual motion, and virtual motion, and only those without a functioning vestibular system are fully immune. The range of vulnerability in the normal population varies about 10,000 to 1. Sleep deprivation can also enhance susceptibility. Systematic studies conducted in parabolic flight have identified velocity storage of semicircular canal signals—velocity integration—as being a key factor in both space motion sickness and terrestrial motion sickness. Adaptation procedures that have been developed to increase resistance to motion sickness reduce this time constant. A fully adequate theory of motion sickness is not presently available. Limitations of two popular theories, the evolutionary and the ecological, are described. A sensory conflict theory can explain many but not all aspects of motion sickness elicitation. However, extending the theory to include conflicts related to visceral afferent feedback elicited by voluntary and passive body motion greatly expands its explanatory range. Future goals should include determining why some conflicts are provocative and others are not but instead lead to perceptual reinterpretations of ongoing body motion. The contribution of visceral afferents in relation to vestibular and cerebellar signals in evoking sickness also deserves further exploration. Substantial progress is being made in identifying the physiological mechanisms underlying the evocation of nausea, vomiting, and anxiety, and a comprehensive understanding of motion sickness may soon be attainable. Adequate anti-motion sickness drugs without adverse side effects are not yet available.

Reducing pain by moving? A commentary on Ferrè et al. 2013

“…Motion sickness is known to affect performances and reaction time already in case of sopite syndrome, i.e. conditions occurring at the onset of motion sickness or in presence of very mild nauseogenic stimuli, in which the symptoms are so low that the participants are often not able to recognize or report them (Lackner, 2014). In our experiment motion sickness was overall very low, but the highest values were found in both left and right optokinetic stimulation conditions, and is plausibly high as well during caloric vestibular stimulation (Ferrè et al, 2013;Ferrè et al, 2015), and could thus have mediated implicit nociceptive processes.…”

“…The sensitivity to motion sickness differs strongly between individuals (Golding & Gresty, 2015;Lackner, 2014). To quantify the possible influence of motion sickness on our results, we monitored its level after each stimulation trial using a simplified Pensacola scale from 0 to 20 (Dai, Kunin, Raphan, & Cohen, 2003).…”

Sleep Duration in Rough Sea Conditions

“…It is known that central nervous system depressants such as promethazine and scopolamine provide protective benefi t against motion sickness, but induce drowsiness. 9 From an operational perspective, we consider the use of such drugs an indirect eff ect of motion sickness that should be taken into account when addressing the operational impact of motion sickness.…”

How Visual Motion Cues Can Influence Sickness For In-Car VR

“…The result is that "anyone with a functional vestibular system can suffer from motion sickness, given the right prerequisites and if the exposure is continuous over a long period" [16] with studies showing that "virtually anyone with normal vestibular function when exposed to provocative physical body motion, disruption of vestibulo-ocular reflexes, or optokinetic stimulation can to some extent be made motion sick". [40]. Thus prevalence tends to be categorised by severity of affliction.…”