Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “MOTION SICKNESS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources
PubMed1998

Modelling motion sickness and subjective vertical mismatch detailed for vertical motions.

In an attempt to predict the amount of motion sickness given any kind of motion stimulus, we describe a model using explicit knowledge of the vestibular system. First, the generally accepted conflict theory is restated in terms of a conflict between a vertical as perceived by the sense organs like the vestibular system and the subjective vertical as determined on the basis of previous experience. Second, this concept is integrated with optimal estimation theory by the use of an internal model. If detailed for vertical motions only, the model does predict typical observed motion sickness characteristics, irrespective the parameter setting. By adjusting the nonvestibular parameters, the model can also quantitatively be adapted to seasickness data from the literature. With this concept, sickness severity hypothetically can also be predicted for other motions, irrespective of their origin and complexity.

Conflict, Psychological↗
PubMed1994

Effects of motion sickness and antimotion sickness drugs on gastric function.

This study examined the effects of motion sickness and antimotion sickness drugs on gastric emptying (GE). Drugs were tested in normal and motion sick subjects. To induce motion sickness, subjects performed head movements while seated in a rotating chair. Gastric emptying of liquid (300 mL) was determined by nuclear medicine techniques, whereas gastric electrical activity, the electrogastrogram (EGG), was monitored from surface (cutaneous) electrodes positioned over the abdominal area. Gastric emptying was severely inhibited at the peak of motion sickness symptoms, but returned to normal 15 minutes later when symptoms abated. In normal (non-motion sick) subjects intramuscular (IM) scopolamine (0.1 mg) and IM promethazine (25 mg) inhibited GE, whereas erythromycin ethylsuccinate (EES) suspension (200 mg) given orally increased GE. When administered to motion sick subjects, IM scopolamine and IM promethazine added slightly, but not significantly, to the inhibition of GE already present. Oral EES did not significantly alter GE in motion sick subjects. Although EGG frequency remained within normal limits (approximately 2.5-3.5 cpm) after liquid ingestion in both normal and motion sick subjects, EGG amplitude was differentially affected in the two groups. Electrogastrogram amplitude increased twofold to fourfold after liquid ingestion in normal, but not in motion sick subjects. The results suggest that (1) maximal inhibition of GE is coincident with peak motion sickness symptoms, (2) both IM scopolamine and IM promethazine inhibit GE in normal subjects, but do not add significantly to the inhibition of GE already established during motion sickness, (3) orally administered erythromycin enhances GE in normal, but not in motion sickness subjects, and (4) the normal stimulatory effect of liquid ingestion on gastric motility does not occur in motion sick subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1988

Neuropsychiatric observations of proprioceptive sensitivity in motion sickness susceptibility.

The assessment of motion sickness susceptibility is still an unsolved problem, due in part to its unclear etiology. We studied 16 referred patients suffering from "idiopathic motion sickness" and 4 pilots suffering from motion airsickness. All clinical and neurological tests proved negative, including electroencephalograms, electronystagmograms, Doppler studies, and computerized tomography of the brain. Cervical spine X-rays and personality characteristics were assessed. Simultaneously, 35 asymptomatic pilots and pilot applicants were studied as controls. Both groups were exposed to cross-coupled accelerations on a Barany chair at 15 rpm along with 0.5 Hz head flexions. The pathological group showed a straightened cervical curvature as well as a significantly higher degree of malaise (scale of Graybiel and Lackner). Their personalities were highly alexithymic or obsessive compared to the control group (Kruskal-Wallis Test). Alexithymic and obsessive personalities may express their stress reactions and psychic conflicts through somatic signs, such as cervical muscle contractures; consequently, straightening the cervical spine with the subsequent alteration of proprioceptive inputs to the vestibular nuclei may increase motion sickness susceptibility.

Adult↗
PubMed2005

Triggers of motion sickness in migraine sufferers.

OBJECTIVE: To determine whether susceptibility to motion sickness provoked by unexpected movement is associated with susceptibility to visually induced motion sickness in migraine sufferers. BACKGROUND: Migraine sufferers are unusually susceptible to motion sickness, but the mechanism of this susceptibility is not well understood. Possibilities include vestibular dysfunction secondary to vasomotor disturbances during migraine attacks, hyperexcitability of brainstem circuits that produce symptoms of motion sickness and migraine, and heightened susceptibility to visual illusions of movement. METHOD: A motion sickness susceptibility questionnaire that listed common triggers of motion sickness was filled out by 42 migraine sufferers and 39 headache-free controls of similar age and sex distribution to migraine sufferers. RESULTS: A greater proportion of migraine sufferers than controls reported that traveling in cars and buses, reading in the car, using playground equipment, watching wide-screen movies and movement simulators, induced motion sickness. However, visually induced motion sickness appeared to be independent of motion sickness to most movement-related stimuli in migraine sufferers. CONCLUSIONS: The lack of association between susceptibility to movement-induced and visually induced motion sickness implies that more than one mechanism increases susceptibility to motion sickness in migraine sufferers.

Adult↗
PubMed2003

The critical role of velocity storage in production of motion sickness.

We propose that motion sickness is mediated through the orientation properties of velocity storage in the vestibular system that tend to align eye velocity produced by the angular vestibulo-ocular reflex (aVOR) with gravito-inertial acceleration (GIA). (GIA is the sum of the linear accelerations acting on the head. In the absence of translational accelerations, gravity is the GIA.) We further postulate that motion sickness produced by cross-coupled vestibular stimulation can be characterized by a metric composed of the disparity between the axis of eye rotation and the GIA, the strength of the response to angular motion, and the response duration, as determined by the central vestibular time constant, that is, by the time constant of velocity storage. The nodulus and uvula of the vestibulocerebellum are likely to be the central sites where the disparity is sensed, where the vestibular time constants are habituated, and where links are made to the autonomic system to produce the symptoms and signs.

Adult↗
PubMed2006

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.

Adaptation, Physiological↗
PubMed1997

Unusual vestibular and visual input in human dynamic balance as a motion sickness susceptibility test.

BACKGROUND: Motion sickness (MS) is commonly thought to arise from a sensory conflict. However, few quantitative methods based on this theory are available to detect MS susceptibility. HYPOTHESIS: It was asked whether the standardized unusual stimulation of a single sensory channel under quantified dynamic balance conditions in man could elicit a sensory conflict and therefore trigger motion sickness (MS) METHODS: Vestibular and visual channels were stimulated by galvanic current and rotating prismatic glasses, respectively. The moving platform used to create the requirements for dynamic balance conditions was chosen not only to worsen the malaise but also to obtain an objective measurement of the balance consequences of the stimulations. RESULTS: Both vestibular and visual stimulation, applied separately, elicited MS-like symptoms (in 56% and 73% of subjects, respectively) and stereotyped balance reactions. A relationship was found between subjective MS-like symptoms and objective measurements of dynamic balance performance. Subjects sensitive to unusual vestibular messages differed from the others by a greater increase in the parameters indicating a difficulty of balance whereas subjects sensitive to unusual visual messages were recognized by the strategy they used to balance themselves. CONCLUSIONS: These results demonstrated that a sensory conflict can trigger MS-like symptoms. We conclude that the measured parameters of a global somatomotor activity, such as the dynamic balance task proposed here, could be useful for objectively detecting subjects predisposed to MS, for training them and testing the efficiency of anti-MS drugs.

Adult↗
PubMed2006

Motion sickness history, food neophobia, and sensation seeking.

Motion sickness is believed to be caused by conflicting sensory signals, a situation that mimics the effects of ingesting certain toxins. Thus, one might suspect that individuals who have experienced a relatively high frequency of motion sickness may be particularly vigilant about avoiding anything that produces nausea, induding potentially nauseating toxins. Consequently, they may be more resistant to trying new foods, i.e., be more food neophobic, since unfamiliar foods can have unexpected adverse effects due to toxins or allergens. Likewise, many highly stimulating experiences can trigger motion sickness, so individuals who are more susceptible may be more prone to avoid such experiences, i.e., be less sensation seeking. Finally, it was expected that food neophobia would be more frequent in individuals low on sensation seeking tendencies. Self-reported motion sickness history in 308 adults (M= 18.8 yr.; SD = 1.6) was correlated with scores on the Arnett Inventory of Sensation Seeking and the Food Neophobia Scale. As predicted, greater history of motion sickness was associated with lower Sensation Seeking scores. Food Neophobia was not correlated with motion sickness history but, as expected, was negatively correlated (r = -.42) with scores on Sensation Seeking. Further research is recommended that measures actual sensitivity to motion sickness.

Adolescent↗
PubMed1987

Reliability of provocative tests of motion sickness susceptibility.

Accurate prediction of space motion sickness is dependent, in part, upon the reliability of terrestrial-based motion sickness susceptibility tests. In the present study, test-retest reliability values were derived from motion sickness susceptibility scores obtained from two successive exposures to each of three tests: 1) Coriolis Sickness Sensitivity Index (CSSI); 2) Staircase Velocity Movement Test (SVMT); and 3) Parabolic Flight Static Chair Test (PSCT). The reliability of the three tests ranged from 0.70 to 0.88. Normalizing values from predictors with skewed distributions improved the reliability. The apparent inconsistency between our finding of high reliability of predictive tests, and previous reports of low correlations between ground-based predictors and space motion sickness may be due to unreliability in assessment of the sickness criterion. Issues of reliability and validity of predictor and criterion measures, and their implications for future development of ground-based predictive tests are discussed in some detail.

Acceleration↗
PubMed1976

Nystagmus, turning sensations, and illusory movement in motion sickness susceptibility.

The relationships of motion sickness susceptibility to nystagmic eye movements, sensations of turning, and duration of the spiral aftereffect were determined with 48 subjects separated into groups on the basis of sex and extremes of motion sickness susceptibility. When subjective alertness levels were controlled, there was no enhancement of elicited nystagmus nor turning sensations in susceptible individuals. However, spiral aftereffect durations were significantly longer in susceptible individuals than in nonsusceptible individuals. The results are interpreted as favoring Graybiel's model of the structural elements in motion sickness.

Adolescent↗
PubMed1983

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.

Adaptation, Biological↗
PubMed1994

Habituation and motion sickness.

The vestibular, cerebellar, and reticular systems are central in importance, in motion sickness and habituation, to the effects of motion. Nuclear medicine single photon emission computed tomography (SPECT) studies of cerebral blood flow and power spectral electroencephalographic recordings during motion sickness were used to determine alterations in the central nervous system. The rotating chair with and without visual stimulation was used to study the rate of habituation and the effect of antimotion sickness medications on this rate. An increase of theta waves over the frontal cortex indicated a decreased activation of the higher centers during motion sickness. Motion sickness also produces an increase of blood flow in the central cerebellum that has connections to the reticular system. This increase in cerebellar activity is relayed to the reticular system whereby neural recruitment builds up to trigger the vomiting center, producing motion sickness. Habituation may be a conditioned compensatory activation of the reticular neurons that prevents this disruption of normal activation. The rate of habituation when motion sickness was prevented by scopolamine was slowed, indicating that, if the central nervous system is not challenged by disruption of normal activation, it does not produce the compensatory reactions that result in habituation.

Adult↗
PubMed2002

Effect of magnitude and direction of horizontal oscillation on motion sickness.

BACKGROUND: Various types of motion and visual scene can cause motion sickness, but sickness in land transport seems to be often associated with variations in horizontal acceleration. If horizontal oscillation causes sickness, it seems reasonable to assume that greater amounts of motion (i.e., an increased magnitude of motion or an increased duration of motion) will increase the extent of the sickness. HYPOTHESIS: It was hypothesized that the magnitude, direction, and duration of horizontal oscillation would affect the sickness experienced by subjects. METHOD: The 144 subjects were exposed to horizontal sinusoidal oscillation at a frequency of 0.315 Hz while seated in a closed cabin with their eyes open for up to 30 min. Subjects were exposed to one of 12 conditions with either fore-and-aft or lateral oscillation at magnitudes of either: (i) 0.28 ms(-2) rms, (ii) 0.56 ms(-2) rms, (iii) 0.70 ms(-2) rms, (iv) 0.89 ms(-2) rms, (v) 1.11 ms(-2) rms, or (vi) a stationary control condition. Subjects provided ratings of their motion sickness symptoms at 1-min intervals during the 30-min exposures. RESULTS: At a frequency of 0.315 Hz, an increase in either the magnitude or the duration of horizontal oscillation resulted in increases in the incidence of motion sickness. There were significant positive correlations between self-ratings of motion sickness susceptibility provided by subjects before participating in the experiment and their illness ratings during the experiment. CONCLUSIONS: At a frequency of 0.315 Hz, motion sickness caused by horizontal oscillation increases with increases in the magnitude and duration of horizontal oscillation. For the conditions of this study, the sickness was similar with fore-and-aft and lateral oscillation.

Acceleration↗
PubMed2000

Motion sickness.

The number of recently published papers on motion sickness may convey the impression that motion sickness is far from being understood. The current review focusses on a concept which tends to unify the different manifestations and theories of motion sickness. The paper highlights the relations between ergonomic principles to minimise motion sickness and the concept predictions. The clinical management of sufferers from motion sickness in terms of selection, pharmacological measures and desensitisation courses is treated as well.

Humans↗
PubMed1983

Etiological factors in space motion sickness.

We compared susceptibility to motion sickness during exposure to sudden-stop stimulation as a function of gravitoinertial force level. Our findings show that susceptibility is greatly enhanced, both with eyes-closed and eyes-open, for zero-g and 2-g conditions in parabolic flight compared with 1-g test conditions. The change in susceptibility is likely related to three factors: alterations in vestibulo-ocular function which result from variations in gravitoinertial force level (28,29); the altered pattern of otolithic activity resulting during variations in gravitoinertial force level; and the altered canal-otolith response synergies that result during exposure to gravitoinertial force levels greater or less than terrestrial levels. These factors are shown to be related to the etiology of space motion sickness and to the alterations in performance and vestibular function that are experienced by astronauts during reentry. An explanation is also proposed for the decrease in susceptibility to motion sickness exhibited by the Skylab astronauts inflight and for some period postflight during exposure to cross-coupled angular accelerations.

Adult↗
PubMed1992

[Clinical study on the mechanism of motion sickness--clinical examination based on trigger factors].

This report deals with factors which trigger motion sickness. The author has focused on the clinical examinations applied to motion sickness cases. Relationships between clinical data and susceptibility to motion sickness were investigated. The following results were obtained: 1. CV R-R(coefficient of variation of R-R intervals on EGG)in the frequent motion sickness group showed higher values than in the occasional motion sickness group. This result suggests a hyperfunction of the vagus nerve. 2. In caloric testing with ENG, the motion sickness group showed lower values of duration and eye speed than the occasional motion sickness group. On the other hand, the frequent group showed higher values of laterality in eye speed than the occasional group. 3. With the visual suppression test, the frequent motion sickness group showed higher values than the occasional motion sickness group. On the other hand, there was a significant difference between the frequent motion sickness group and the occasional motion sickness group in terms of laterality of visual suppression values. 4. In testing fluctuation of CV R-R in response to optokinetic stimuli, the frequent motion sickness group showed elevation of CV R-R values after optokinetic load. On the other hand, the occasional motion sickness group showed depression of CV R-R values after the same load. 5. Among clinical examinations designed to diagnose susceptibility to motion sickness, CV R-R, the caloric test, the visual suppression test and OKP testing can produce sufficiently accurate results for clinical investigation.

Electrocardiography↗
PubMed2002

Spatial task performance, sex differences, and motion sickness susceptibility.

There are substantial individual differences in susceptibility to motion sickness, yet little is known about what mediates these differences. Spatial ability and sex have been suggested as possible factors in this relationship. 89 participants (57 women) were administered a Motion Sickness Questionnaire that assesses motion sickness susceptibility, a Water-level Task that gauges sensitivity to gravitational upright, and a Mental Rotation Task that tests an individual's awareness of how objects typically move in space. Significant sex differences were observed in performance of both the Water-level Task (p<.01), and the Mental Rotation Task (p<.005), with women performing less accurately than men. Women also had significantly higher scores on the Motion Sickness Questionnaire (p<.005). Among men, but not women, significant negative relationships were observed between Water-level Task performance and Motion Sickness Questionnaire score (p<.001) and between Mental Rotation Task performance and Motion Sickness Questionnaire score (p<.005). In conclusion, women performed significantly more poorly than men did on the spatial ability tasks and reported significantly more bouts of motion sickness. In addition, men showed a significant negative relationship between spatial ability and motion sickness susceptibility.

Adolescent↗
PubMed2005

Motion sickness is linked to nystagmus-related trigeminal brain stem input: a new hypothesis.

Motion sickness is a common and distressing but poorly understood syndrome associated with nausea/vomiting and autonomic nervous system accompaniments that develops in the air or space as well as on sea or land. A bidirectional aetiologic link prevails between migraine and motion-sickness. Motion sickness provokes jerk nystagmus induced by both optokinetic and vestibular stimulation. Fixation of gaze or closure of eyes generally prevents motion sickness while vestibular otolithic function is eliminated in microgravity of space, indicating a predominant pathogenetic role for visuo-sensory input. Scopolamine, dimenhydrinate, and promethazine reduce motion-related nystagmus. Contraction of extraocular muscles generates proprioceptive neural traffic and can provoke an ocular hypertensive response. It is proposed that repetitive contractions of the extraocular muscles during motion-related jerk nystagmus rapidly augment brain stem afferent input by increasing proprioceptive neural traffic through connections of the oculomotor nerves with the ophthalmic nerve in the lateral wall of the cavernous sinus as well as by raising the intraocular pressure thereby stimulating anterior segment ocular trigeminal nerve fibers. This verifiable hypothesis defines the pathophysiological basis of individual susceptibility to motion sickness, elucidates the preventive mechanism of gaze fixation or ocular closure, advances the aetiologic link between MS and migraine, rationalizes the mechanism of known preventive drugs, and explores new therapeutic possibilities.

Afferent Pathways↗