Motion sickness and anxiety

Ninety-four Israeli pilot trainees completed a battery of anxiety related questionnaires: Taylor Manifest Anxiety Scale, EPQ, 16PF, and Spielberger's State and Trait Anxiety Scores. Self reports and flight instructor observations of motion sickness symptoms were collected after initial flights. No significant correlations were found between these two sources. Anxiety scores derived from the battery of anxiety questionnaires were correlated with self reports of motion sickness but not with instructor observations. Discussion focused on the potential limitations of external observers in assessing motion sickness, the convergence of anxiety assessments, and the overlap between anxiety and motion sickness symptoms. Methodological and practical implications conclude the review.     

Motion sickness in the squirrel monkey

Because it is of the same taxonomic order as man, the squirrel monkey has been introduced as a nonhuman primate model for the study of such aspects of motion and space sickness as susceptibility, prevention, treatment, and neural mechanisms. In this study on susceptibility, the specific aims were to examine the effects of combined vertical rotation and horizontal acceleration, phenotype, sex, visual cues, morning and afternoon testing, and repeated test exposures on incidence, frequency, and latency of emetic responses. The highest emetic incidence of 89%, with an emetic frequency of 2.0, during 60 min, and a latency of 19 min from onset of testing, occurred at 25 rpm and 0.5 Hz linear acceleration. Susceptibility--defined by incidence, frequency, and/or latency of emesis--was significantly higher in Bolivian than Colombian phenotypes, in the presence of visual cues, in males, but not at different periods of the day or with two successive test exposures. Since the emetic responses were quite similar to man in the eliciting motion stimuli, it was concluded that the squirrel monkey represents a very suitable primate model for studies of motion and space sickness.     

Motion sickness and equilibrium ataxia.

In order to know the relationship between motion sickness and equilibrium ataxia, we performed Graybiel's ataxia test battery on 10 normal subjects: 1) before donning goggles which reversed the optical image horizontally and vertically; 2) while wearing the goggles and walking; and 3) after walking as long as possible up to 90 min. Horizontal reversal of vision resulted in a statistically significant decrease in the score for all the closed-eyes tests and one open-eyes test performed during walking and after walking, respectively. In contrast, walking while wearing vertical reversing goggles produced a significant but very small change for one of the closed-eyes tests alone. The present study indicates that failure to detect spatial orientation, which evokes autonomic nervous symptoms as an alarm sign, produces equilibrium ataxia by impairing the top-down regulation of body balance, and that vertically reversed vision does not impair spatial orientation needed to maintain upright posture or to execute locomotion.     

Motion sickness induced by optokinetic drums

Motion sickness is not only elicited by certain kinds of self-motion, but also by motion of a visual scene. In case of the latter, optokinetic drums are often used and a visual-vestibular conflict is assumed to cause the sickness. When the rotation axis is Earth vertical however, different studies show different results. Here, we propose that visual-vestibular conflicts per se do not cause sickness whereas subjective vertical mismatch theory can reconcile the disparate findings. The theory attributes the nausea induced by horizontal optokinetic stimulation to the subjects self-inducing pseudo-Coriolis by head movement. This highlights the shortcomings of an optokinetic apparatus--that is non-rigid or inaccurately oriented--and the importance of constraining the subject's behavior.     

Melatonin and zopiclone as facilitators of early circadian sleep in operational air transport crews

INTRODUCTION: This study was an extension into an operational setting of previous laboratory work investigating the use of zopiclone and melatonin to facilitate early circadian sleep in transport aircrew. The previous laboratory-based study demonstrated that both melatonin and zopiclone were effective in inducing early circadian sleep without impacting on psychomotor performance after a 7-h sleep period. METHODS: In a repeated measures, placebo-controlled protocol, 30 aircrew flew 3 transatlantic missions over which they took each of the 3 medications (placebo, sustained-release melatonin 2 mg, or zopiclone 5 mg) at an early body clock time (17:00) during their first stopover. They wore wrist actigraphs prior to and throughout the missions, took a single dose of their scheduled medication immediately prior to their early circadian bedtime, and completed a sleep questionnaire on arising from their medicated sleep. RESULTS: The results of the actigraphic data show that relative to placebo, aircrew on melatonin and zopiclone fell asleep more quickly (melatonin: p < 0.01, zopiclone: p < 0.003), slept more (melatonin: p < 0.02, zopiclone: p < 0.005), had fewer awakenings after sleep onset (melatonin: p < 0.004, zopiclone: p < 0.01), and spent less time awake after sleep onset (melatonin: p < 0.01, zopiclone: p < 0.05). The results of the questionnaire data show that relative to placebo, aircrew on melatonin and zopiclone experienced less difficulty getting to sleep (melatonin: p < 0.0001, zopiclone: p < 0.001), had fewer awakenings (melatonin: p < 0.005, zopiclone: p < 0.001), less difficulty returning to sleep after awakening (melatonin: p < 0.0001, zopiclone: p < 0.0001), and reported a better sleep quality (melatonin: p < 0.0003, zopiclone: p < 0.0004). There were no statistically significant differences between melatonin and zopiclone in any of the actigraphic or questionnaire sleep parameters. CONCLUSIONS: Melatonin and zopiclone, in the dosages we used, are equipotent facilitators of early circadian sleep during transmeridian air transport operations.     

Decompression sickness: USN operational experience 1969-1989.

This report presents data on the U.S. Navy's experience in decompression sickness occurring in operational flight from 1 January 1969 to 30 December 1989. During these 21 years, decompression sickness was reported in 12 USN aircraft and involved 15 aircrew. The primary cause of decompression, as might be expected, was a loss of cabin or cockpit pressurization. The most common manifestation of decompression sickness was limb or joint pain although some crewmembers experienced various manifestations of neurological dysfunction. One crewmember experienced chokes. Of the 15 afflicted aircrew, 13 (87%) had complete remission of symptoms by the time they landed. Two crewmembers required compression therapy for resolution of symptoms. None of the reported symptoms were incapacitating and none of the aircraft involved crashed or received even minor damage.     

Motion sickness susceptibility fluctuates through the menstrual cycle

INTRODUCTION: Surveys of transportation by sea, land, and air indicate that women are more susceptible to motion sickness than men, showing higher incidences of vomiting and reporting more symptoms such as nausea. The cause of this greater motion sickness susceptibility in women is unknown. One suggestion is that it is due to the functioning of the female endocrine system, but there are contradictions between existing studies. HYPOTHESIS: Motion sickness in women varies across the menstrual cycle. METHODS: There were 12 healthy women, age 24.4 +/- 6.6 yr (mean +/- SD), not using contraceptive medication, who were exposed to a provocative cross-coupled (Coriolis) motion continued to the point of moderate nausea. The motion stimulus was whole body rotation on a turntable, during which subjects executed head tilts of approximately 45 degrees in batches of eight spaced at 30-s intervals during a staircase profile of rotational velocity which commenced from stationary and incremented in steps of 3 degrees x s(-1) every 30 s. Subjects were tested on: A.) day 5 'menstruation'; B.) day 12 'ovulatory'; C.) day 19 'mid-luteal'; and D.) day 26 'pre-menstrual,' according to a design counter-balanced for order. RESULTS: Mean +/- SD sequences of head movements required to achieve moderate nausea were: A.) 13.7 +/- 2.8; B.) 14.3 +/- 4.5; C.) 15.4 +/- 6.6; and D.) 16.9 +/- 6.1. The difference between A and D was significant (p < 0.05, 2-tailed). CONCLUSIONS: There was a trend indicating that motion sickness susceptibility was maximal at day 5 'menstruation', decreasing through days 12 and 19 to a minimum at day 26 'pre-menstrual', to a small but significant extent. However, it is unlikely that this can fully account for the greater susceptibility in women since the magnitude of fluctuation in susceptibility across the cycle is only around one-third of the overall difference between male and female susceptibility.     

Motion sickness susceptibility in parabolic flight and velocity storage activity

In parabolic flight experiments, we have found post-rotary nystagmus to be differentially suppressed in free fall (OG) and in a high gravitoinertial force (1.8G) background relative to 1G. In addition, the influence of postrotary head movements on nystagmus suppression was found to be contingent on G level. The nature of this pattern indicated a G-dependency of the velocity storage and dumping mechanisms. Here, we have rank-correlated susceptibility to motion sickness during head movements in OG and 1.8G with the following: a) the decay time constant of the slow phase velocity of post-rotary nystagmus under 1G, no head movement, baseline conditions, b) the extent of time constant reduction elicited in OG and 1.8G; c) the extent of time constant reduction elicited by head tilts in 1G; and d) changes in the extent of time constant reduction in OG and 1.8G over repeated tests. Susceptibility was significantly correlated with the extent to which a head movement reduced the time constant in 1G, was weakly correlated with the baseline time constant, but was not correlated with the extent of reduction in OG or 1.8G. This pattern suggests a link between mechanisms evoking symptoms of space motion sickness and the mechanisms of velocity storage and dumping. Experimental means of evaluating this link are described.     

Motion sickness decreases arterial pressure and therefore acceleration tolerance

BACKGROUND: Motion sickness is a common aeromedical problem that may occur in pilots exposed to increased gravitoinertial load in the head-to-foot direction (+Gz). Since motion sickness may affect autonomic nervous functions including cardiovascular control, it was hypothesized that it might interfere with cardiovascular responses to high +Gz, thereby decreasing G tolerance. METHODS: G tolerance and cardiovascular responses to increased G load were studied in nine subjects in a centrifuge environment under two conditions. In the motion sickness condition, the subject was exposed to a motion sickness provocation (MSP) comprising repeated rapid changes in G load in combination with a regimen of head movements. In the control condition the subject was exposed to similar cumulative G-time stress, but without the MSP. Mean arterial pressure (MAP) was measured. An index of peripheral vascular resistance was achieved by measuring the difference in skin temperature between the forearm and fingertip (deltaT(forearm-fingertip)). RESULTS: MSP decreased gradual-onset rate G tolerance from 5.1 +/- 1.0 G (mean +/- SD) to 4.6 +/- 0.9 G. There was no change in gradual-onset rate G tolerance in the control condition. Rapid-onset rate G tolerance was lower in the motion sickness (2.9 +/- 0.5 G) than in the control (3.4 +/- 0.3 G) condition. MSP reduced MAP by 11 mmHg and deltaT(forearm-fingertip) by 4.2 +/- 4.1 degrees C. In the control condition MAP and deltaT(forearm-fingertip) were unaffected. CONCLUSIONS: Motion sickness may reduce the arterial pressure response to the extent that the capacity of an individual to withstand increased G loads in the head-to-foot direction is significantly diminished.     

Motion sickness: effect of the frequency of lateral oscillation

INTRODUCTION: Low-frequency lateral oscillation is a cause of motion sickness in some forms of transport. However, the relationship between occurrence of sickness and the frequency of lateral oscillation is not known. This paper presents a study of motion sickness with lateral oscillation at frequencies between 0.0315 Hz and 0.20 Hz. METHOD: There were 120 subjects, in 6 groups of 20, who were exposed for up to 30 min to sinusoidal lateral oscillation with a peak velocity of 1.0 ms(-1) at one of six frequencies (0.0315, 0.05, 0.08, 0.125, 0.16, 0.20 Hz). Subjects provided ratings of their motion sickness symptoms at 1-min intervals. RESULTS: There was a highly significant effect of the frequency of lateral oscillation on the occurrence of mild nausea. DISCUSSION: The present results have been combined with those from a previous experiment conducted with higher frequencies of oscillation to produce a frequency weighting for motion sickness caused by lateral oscillation over the range 0.0315 to 0.8 Hz. CONCLUSIONS: Mild nausea caused by lateral oscillation may be predicted by an acceleration frequency weighting that is independent of frequency from 0.0315 to 0.25 Hz and reduces at 12 dB per octave (i.e., proportional to displacement) from 0.25 to 0.8 Hz. This weighting differs from the frequency weighting currently used for predicting motion sickness caused by vertical oscillation. The frequency weighting for lateral oscillation may not be applicable in those environments in which there is roll motion during lateral oscillation.     

Motion sickness severity under interaction of vection and head movements

Vection alone, or combined with head movements, has been shown to invoke motion sickness (MS). This study's purpose was to observe how different combinations of vection and head movements influenced the severity of MS. We tested 26 subjects in a rotating sphere at a speed of 45 degrees/s, resulting in vertical yaw, horizontal roll or pitch vection. Coincidently, subjects pitched, rolled, or yawed their heads (0.5 Hz, 20 degrees). We found that yaw vection combined with pitch or roll head movements significantly increased MS, while pitch vection with any type of head movement, or head and scene rotation about the same axis significantly reduced MS. When the head was kept stationary, pitch vection was most stressful for MS, followed by roll vection, then yaw vection, although yaw vection was the strongest sensation of self-rotation.     

Motion sickness susceptibility and aerobic fitness: a longitudinal study

A longitudinal study evaluated the susceptibility to motion sickness in initially unfit subjects before and after an endurance training program. Motion stimulation was provided by the Precision Angular Mover, in which the subject was tumbled head over heels about an Earth-horizontal axis at 20 cycles per minute in darkness. Maximal aerobic power and the blood lactate response to submaximal exercise were evaluated with cycle ergometry. The training program caused significant improvements in VO2max and endurance capacity, and a significant decrease in percent body fat. There was a significant (p less than 0.0125) increase in motion sickness susceptibility after the physical training, suggesting that increased physical fitness caused increased susceptibility to motion sickness in some individuals.     

倒视诱发运动病及其适应效应

目的观察倒视诱发运动病的敏感性和适应性特点，为从反应敏感性和适应性两方面改进运动病易感性检测方法提供依据。方法受试者１２名，每人做：①倒视加头动试验：戴倒视镜面对视野做规定的头动，有明显恶心感即终止。在不同的日期重复该试验５次。②平行秋千摆动试验：秋千的摆长６ｍ，摆角４５°。出现明显的恶心感即终止。秋千试验在倒视头动系列试验前、后一周各做１次。根据头动套数、摆动时间和症状分值，分别计算两种运动病的敏感性指数（ＭＳＳＩ）。结果①倒视运动病发生率为８３．３％。主要症状为头晕和恶心综合征。②在重复倒视头动试验中的ＭＳＳＩ均值逐次增加，有明显的适应效应。③倒视试验后秋千试验的ＭＳＳＩ值比前一次的值有所提高，表现出适应性由倒视刺激向秋千刺激的转移现象。④倒视加头动与平行秋千诱发运动病敏感性比较，两者有明显的一致性；而运动病的敏感性与适应性之间无明显一致。结论倒视诱发运动病敏感性与基础的秋千运动病敏感性基本一致。人体对重复倒视刺激有明显的适应效应，并有一定的可转移性。倒视加头动刺激方法简便易行，是检测个体运动病敏感性和适应性的较好方法。     

Motion sickness during fore-and-aft oscillation: effect of the visual scene

BACKGROUND: Repetitive braking and acceleration can cause carsickness, with the extent of sickness depending on the forward view outside the car. HYPOTHESIS: It was hypothesized that the visual scene would influence motion sickness caused by low-frequency, low-magnitude fore-and-aft oscillation in the laboratory. METHOD: There were 120 seated male subjects who were exposed to 30 min of 0.1-Hz fore-and-aft oscillation at an acceleration magnitude of 0.89 m x s(-2) rms (a displacement of +/- 3.18 m). Subjects sat in a cabin with one of six scenes: 1) an internal view of two-dimensional black shapes on a white background; 2) an external view of the same two-dimensional shapes; 3) an external view of six horizontal black lines; 4) a 'real' three-dimensional external view; 5) no view (blindfolded); or 6) an internal collimated view of the two-dimensional shapes. Due to practical constraints, only conditions 1, 2, and 6 were tested in a balanced order. Ratings of motion sickness were obtained at 1-min intervals. RESULTS: Each of the six conditions caused motion sickness, with mean illness ratings that increased similarly over time regardless of viewing condition. The symptoms did not differ significantly between conditions and there was no difference in the risk of reaching an illness rating of 2, 'mild symptoms,' between the six viewing conditions. DISCUSSION AND CONCLUSIONS: With a larger number of subjects, a small mean effect of vision might be found with motions having similar frequencies or similar magnitudes to the conditions investigated here. Nevertheless, compared with the large effects of vision with some motions, it is concluded that the visual scene has little effect on sickness caused by pure fore-and-aft oscillation at a frequency of 0.1 Hz and an acceleration magnitude of 0.89 m x s(-2) rms.     

Motion sickness: advances in pathogenesis, prediction, prevention, and treatment

Motion sickness has a major influence on modern traveling activities and the rapidly spreading engagement in virtual reality immersion. Recent evidence emphasizes the role of the otoliths in the pathogenesis of motion sickness, and several new theories may help explain its occurrence beyond the traditional sensory conflict theory. A promising new direction is the recently reported association of genetic polymorphism of the alpha2-adrenergic receptor with increased autonomic response to stress and motion sickness. Various physiological measures for the evaluation and prediction of motion sickness have been tested. However, no single parameter has yet been found to be of high enough sensitivity and specificity for the diagnosis or prediction of individual motion sickness susceptibility. A number of pharmacological and non-pharmacological countermeasures are used for the prevention and treatment of motion sickness. The non-pharmacological options include all procedures that reduce conflicting sensory input, accelerate the process of multi-sensory adaptation, and promote psychological factors which enable the subject to cope with his/her condition. The most effective anti-motion sickness drugs are central acting anticholinergics and H1 antihistamines; however, adverse effects on psychomotor performance may limit their use in drivers, pilots, and naval crewmembers. Recent studies may be relevant to our understanding of the link between motion sickness, migraine, vertigo, and anxiety. Based on these findings and on recent neurochemical data, the development of new anti-motion sickness agents is a promising field of investigation.     

Motion sickness provoked by torso rotation predicts that caused by head nodding

INTRODUCTION: Some degree of space motion sickness is experienced by at least 50% of astronauts early in flight. It is unpleasant and could be hazardous during an extravehicular activity or urgent re-entry in the first few days after launch. To date, there is no reliable ground-based test to predict who will be affected. METHODS: Head nodding (HN) in a supine position was used as a model of motion sickness caused by an unusual gravito-inertial environment. Torso rotation (TR) was used as a means of predicting susceptibility to development of symptoms caused by HN. Motion sickness was quantified in 26 subjects (5 men, 21 women, age range 18-52) using numerical estimates of discomfort and a more detailed questionnaire. Susceptibility to TR and HN was determined on three occasions for each stimulus, with test sessions at least 1 mo apart. RESULTS: Subjects reached their stopping point at a mean duration of 13.72 min +/- 1.06 CI) for TR and 11.31 min (+/- 0.38 CI) for HN. When susceptibility to HN was plotted as a function of susceptibility to TR and a linear regression line was added, the correlation coefficient was 0.744. DISCUSSION: Susceptibility to TR predicts susceptibility to HN. The method may be useful as a screening test for potential astronauts.     

Motion sickness: effect of the magnitude of roll and pitch oscillation

BACKGROUND: Rotational oscillation in roll and pitch can cause motion sickness, but it is not known how sickness depends on the magnitude of rotational oscillation or whether there is a difference between the two axes of motion. HYPOTHESIS: It was hypothesized that motion sickness would increase similarly with increasing magnitudes of roll and pitch oscillation. METHOD: There were 120 subjects (6 groups of 20 subjects) who were exposed to 30 min of 0.2-Hz sinusoidal roll or pitch oscillation at 1 of 3 magnitudes: 1) +/- 1.830; 2) +/- 3.66 degrees; or 3) +/- 7.32 degrees. Subjects sitting in a closed cabin with their eyes open gave ratings of their illness on a 7-point illness rating scale at 1-min intervals. RESULTS: Over the six conditions, mild nausea was reported by 17.5% of subjects. With both roll oscillation and pitch oscillation, mean illness ratings were least with +/- 1.83 degrees of rotational oscillation and greater with +/- 3.66 degrees and +/- 7.32 degrees of oscillation. At none of the three magnitudes of oscillation was there a significant difference in motion sickness caused by roll and pitch oscillation. CONCLUSIONS: With rotational oscillation about an Earth-horizontal axis, there is a trend for motion sickness to increase with increasing motion magnitude. For the conditions investigated, similar motion sickness was caused by roll and pitch oscillation.     

Motion sickness: acquisition and retention of adaptation effects compared in three motion environments

A sharp distinction should be made between symptoms of motion-sickness per se and phenomena inferred from the symptomatology, which include rates of acquisition and decay of adaptation effects. Foreknowledge of these "derived phenomena" are valuable if it can be shown that they hold true for virtually any motion environment. Recently, we have developed a sudden-stop vestibulovisual interaction test for measuring susceptibility to motion sickness (1). The test procedure involves four successive assessments that provide not only an index of susceptibility to motion sickness but also the rates of acquisition and decay of adaptation effects. The 14 subjects participating in this test had previously served as subjects in parabolic flight experiments and seven of them had also taken part in the assessment of antimotion-sickness remedies in a slow rotation room. The present report examines whether their rates of acquisition and decay of adaptation to stressful motion represent consistent general features of their responses across motion environments. From these comparisons, it appears that an individual's rates of acquiring and losing adaptation are quite consistent in very different situations. The pattern of results also suggests modifications of the sudden-stop vestibulovisual test that should increase its effectiveness as a motion-sickness screening procedure, both for orbital flight and for terrestrial conditions.