Showing papers on "Motion sickness published in 1998"
TL;DR: It was concluded that the revised MSSQ can be used as a direct replacement of the original version and points to the involvement of the vestibular system in the response to nonmotion emetogenic stimuli.
411 citations
TL;DR: Analysis of postural motion during exposure to the moving room revealed increases in postural sway before the onset of subjective motion sickness symptoms, which confirms a key prediction of the postural instability theory of motion sickness.
292 citations
TL;DR: Effective drugs for combating motion sickness include antihistamines, antimuscarinics, 5-HT1A (serotonergic) receptor agonists and neurokinin type 1 receptor antagonists, but considerable information concerning the physiological basis and pharmacology of motion sickness is unknown.
211 citations
TL;DR: This article summarizes a variety of newly published findings obtained by the Neuroscience Laboratory, Johnson Space Center, and attempts to place this work within a historical framework of previous results on posture, locomotion, motion sickness, and perceptual responses that have been observed in conjunction with space flight.
189 citations
TL;DR: In an attempt to predict the amount of motion sickness given any kind of motion stimulus, a model is described using explicit knowledge of the vestibular system and is integrated with optimal estimation theory by the use of an internal model.
173 citations
TL;DR: It is suggested that deficient perceptual-motor responses to disorienting conditions may contribute to motion sickness susceptibility.
87 citations
01 Jan 1998
TL;DR: In this article, a framework is presented for comprehending partly participants' spatial perception in virtual environments and the sense of presence, or of "being in" a virtual environment, should be increased bv manipulations that facilitate perception of a virtual scene as a perceptual rest frame.
Abstract: A framework is presented for comprehending partly participants' spatial perception in virtual environments. Specific hypotheses derived from that framework include: simulator sickness should be reducible through visual background manipulations; and the sense of presence, or of "being in" a virtual environment, should be increased bv manipulations that facilitate perception of a virtual scene as a perceptual rest frame. Experiments to assess the simulator sickness reduction hypothesis demonstrated that congruence between the visual background and inertial cues decreased reported simulator sickness and per-exposure postural instability. Experiments to assess the presence hypothesis used two measures: self-reported presence and visual-inertial nulling. Results indicated that It meaningful virtual scene, as opposed to a random one, increased both reported presence and the level of inertial motion required to overcome perceived self-motion elicited by scene motion. The simulator sickness research implies that visual background manipulations may be a means to reduce the prevalent unwanted side-effects of simulators. The presence research introduces a procedure, possibly based on brain-stem level neural processing, to measure the salience of virtual environments. Both lines of research are central to developing effective virtual interfaces which have the potential to increase the human-computer bandwidth, and thus to partially address the information explosion.
79 citations
TL;DR: The widespread occurrence of motion sickness in both experiments clearly confirmed the main hypothesis of sensory conflict theory and evidence relating to the subsidiary proposition of sensory Conflict theory was inconsistent.
76 citations
TL;DR: Differences in the sensitivity of postural stability measurement techniques and variations in inter- and intraindividual responses to measures are demonstrated and correlation was found between reports of simulator sickness and balance-related symptoms.
75 citations
TL;DR: The sopite syndrome is a poorly understood response to motion that can exist in isolation from more apparent symptoms such as nausea, can last long after nausea has subsided, and can debilitate some individuals.
73 citations
TL;DR: It is indicated that pitch and roll when combined with small heave motions, which in themselves are not sickness provoking, produce more motion sickness than claimed by the classic models.
TL;DR: Since there is considerable individual variation in postflight deficit and since adaptation from prior flights seems to persist, it has been recommended that commanders with prior shuttle landing experience be named to flights of extended duration.
Abstract: Space motion sickness is a well-recognized problem for space flight and affects 73% of crewmembers on the first 2 or 3 days of their initial flight. Illness severity is variable, but over half of cases are categorized as moderate to severe. Management has included elimination of provocative activities and delay of critical performance-related procedures such as extra-vehicular activity (EVA) or Shuttle landing during the first three days of missions. Pharmacological treatment strategies have had variable results, but intramuscular promethazine has been the most effective to date with a 90% initial response rate and important reduction in residual symptoms the next flight day. Oral prophylactic treatment of crewmembers with difficulty on prior flights has had mixed results. In order to accommodate more aggressive pharmacologic management, crew medical officers receive additional training in parenteral administration of medications. Preflight medication testing is accomplished to reduce the risk of unexpected performance decrements or idiosyncratic reactions. When possible, treatment is offered in the presleep period to mask potential treatment-related drowsiness. Another phenomenon noted by crewmembers and physicians as flights have lengthened is readaptation difficulty or motion sickness on return to Earth. These problems have included nausea, vomiting, and difficulty with locomotion or coordination upon early exposure to gravity. Since landing and egress are principal concerns during this portion of the flight, these deficits are of operational concern. Postflight therapy has been directed at nausea and vomiting, and meclizine and promethazine are the principal agents used. There has been no official attempt at prophylactic treatment prior to entry. Since there is considerable individual variation in postflight deficit and since adaptation from prior flights seems to persist, it has been recommended that commanders with prior shuttle landing experience be named to flights of extended duration.
TL;DR: The authors experience vigorous vestibular stimulation when they run, jump, or dance, but these activities almost never make us sick; some forms of motion sickness were recognized in which head and body motion is normal or even absent (flight simulator and Cinerama sickness).
Abstract: Motion sickness is a well-known nausea and vomiting syndrome whose physical signs include vomiting and retching, pallor, cold sweating, yawning, belching, flatulence, and decreased gastric tonus. Subjective symptoms include stomach discomfort, nausea, headache, feeling of warmth, and drowsiness. The research literature has been well reviewed (1-7). Over the past hundred years, our perspective on the kinds of sensory stimulation that can cause motion sickness has broadened considerably. Originally it was assumed that motion sickness can only be caused by motion and is due to mechanical stimulation of visceral afferents or changes in cerebral blood flow caused by body motion. It was eventually recognized that people who have no inner ear balance organ function are totally immune, indicating that the malady results specifically from vestibular over-stimulation. However, by 1970 it became apparent that a more comprehensive etiologic framework was needed: some forms of motion sickness were recognized in which head and body motion is normal (that is, spectacle sickness, space sickness) or even absent (flight simulator and Cinerama sickness). We experience vigorous vestibular stimulation when we run, jump, or dance, but these activities almost never make us sick. Claremont (8) had originally suggested that mo-
TL;DR: It is found that caloric stimulation severe enough to produce nystagmus, dizziness, and nausea had no effect on sympathetic nerve activity measured directly with microneurography, and no effect was observed on heart rate, blood pressure, or plasma norepinephrine.
Abstract: There is substantial evidence that anatomical connections exist between vestibular and autonomic nuclei. Animal studies have shown functional interactions between the vestibular and autonomic systems. The nature of these interactions, however, is complex and has not been fully defined. Vestibular stimulation has been consistently found to reduce blood pressure in animals. Given the potential interaction between vestibular and autonomic pathways this finding could be explained by a reduction in sympathetic activity. However, rather than sympathetic inhibition, vestibular stimulation has consistently been shown to increase sympathetic outflow in cardiac and splanchnic vascular beds in most experimental models. Several clinical observations suggest that a link between vestibular and autonomic systems may also exist in humans. However, direct evidence for vestibular/autonomic interactions in humans is sparse. Motion sickness has been found to induce forearm vasodilation and reduce baroreflex gain, and head down neck flexion induces transient forearm and calf vasoconstriction. On the other hand, studies using optokinetic stimulation have found either very small, variable, or inconsistent changes in heart rate and blood pressure, despite substantial symptoms of motion sickness. Furthermore, caloric stimulation severe enough to produce nystagmus, dizziness, and nausea had no effect on sympathetic nerve activity measured directly with microneurography. No effect was observed on heart rate, blood pressure, or plasma norepinephrine. Several factors may explain the apparent discordance of these results, but more research is needed before we can define the potential importance of vestibular input to cardiovascular regulation and orthostatic tolerance in humans.
TL;DR: A distinct pattern was found in the occurrence of motion sickness and headache that related to the menstrual cycle, although motion sick and headache did not generally occur together in most of the subjects.
TL;DR: A vector analysis of the consequences of head movements during somatosensory, visual and/or vestibular rotatory motion stimulation revealed that the more the sensed angular velocity vector after the head movements is aligned with the gravitoinertial force vector, the less nauseating effects are experienced.
TL;DR: Electrogastrography has been used as an objective measure of epigastric symptoms and nausea experienced in visually induced sickness provoked by circularvection and its relation to motion sickness and the underlying mechanism remains unclear.
TL;DR: This conceptual model "explains" why motion sickness is associated with adaptation to novel environments and is in general consistent with motion sickness literature.
TL;DR: These findings do not support the notion that moderate motion sickness is manifested as a generalized autonomic response and are unable to demonstrate a change in autonomic control of heart rate due to rotation alone or due to motion sickness.
Abstract: In a study of 18 human subjects, we applied a new technique, estimation of the transfer function between instantaneous lung volume (ILV) and instantaneous heart rate (HR), to assess autonomic activity during motion sickness. Two control recordings of ILV and electrocardiogram (ECG) were made prior to the development of motion sickness. During the first, subjects were seated motionless, and during the second they were seated rotating sinusoidally about an earth vertical axis. Subjects then wore prism goggles that reverse the left-right visual field and performed manual tasks until they developed moderate motion sickness. Finally, ILV and ECG were recorded while subjects maintained a relatively constant level of sickness by intermittent eye closure during rotation with the goggles. Based on analyses of ILV to HR transfer functions from the three conditions, we were unable to demonstrate a change in autonomic control of heart rate due to rotation alone or due to motion sickness. These findings do not support the notion that moderate motion sickness is manifested as a generalized autonomic response.
TL;DR: Vestibular dysfunction has additionally been linked with anxiety disorders, such as agoraphobia, which may result from alteration of vestibular inputs to brain stem monoaminergic neurons (which are known to process these signals), and sleep disturbances might be connected with Vestibular disorders because neurons in the pontine reticular formation that are critical in switching between sleep states may be influenced by labyrinthine inputs.
Abstract: The vestibular system provides inputs to many neurons in the brain stem that participate in autonomic control. This multiplicity of vestibular-autonomic connections plays a variety of roles. Whereas it has been known for decades that unilateral vestibular lesions can result in motion sickness, recent data suggest that the vestibular system participates in making adjustments in blood pressure and respiration that are necessary to maintain homeostasis during movement and changes in posture. Animals with bilateral vestibular lesions are more susceptible to posturally related hypotension than vestibularly intact animals, and it is also possible that orthostatic hypotension after space flight is caused in part by microgravity-related changes in otolith function. Patients with vestibular lesions could also be more vulnerable to respiratory disturbances related to posture, such as obstructive apnea. Vestibular dysfunction has additionally been linked with anxiety disorders, such as agoraphobia, which may result from alteration of vestibular inputs to brain stem monoaminergic neurons (which are known to process these signals). Even sleep disturbances might be connected with vestibular disorders because neurons in the pontine reticular formation that are critical in switching between sleep states may be influenced by labyrinthine inputs. Thus it is likely that vestibular damage will result in a number of parallel disturbances in autonomic function.
TL;DR: In an experiment with 17 subjects, interactions of visual roll motion stimuli and vestibular body tilt stimuli were examined in determining the subjective vertical and despite the conflicting sensory information, motion sickness was not reported apart from one subject on one single occasion.
TL;DR: A 55% degree of tilt compensation of the lateral acceleration instead of the normal 70% reduced the symptoms of motion sickness incidence (SMSI) by 25-40%.
TL;DR: Inflight and post-landing "immunity" to the "coriolis sickness susceptibility test" suggests that the otolith organs play a major role in space motion sickness, and data indicate that sensory-motor adaptation to microgravity includes a process whereby central interpretation of otolith signals is biased from "tilt" toward translation.
Abstract: Inflight and post-landing "immunity" to the "coriolis sickness susceptibility test", observed during the Skylab M131 experiment, suggests that the otolith organs play a major role in space motion sickness (SMS). This view is supported by the report that ocular counter-torsion asymmetries correlate with SMS incidence and severity. Further data indicate that sensory-motor adaptation to microgravity includes a process whereby central interpretation of otolith signals is biased from "tilt" toward translation. However, unexpected responses to linear acceleration suggest the importance of graviceptors distributed throughout the body in addition to the vestibular otolith organs. Research is needed to assess distributed graviceptor effects.
TL;DR: A new and unanticipated instance of the latter is reported of motion sickness in the absence of imposed motion in a study of spontaneous standing postural sway, and possible implications are considered for the sensory conflict theory and the postural instability theory.
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TL;DR: It is demonstrated that more rapid eye movement indexed by higher frequency of optokinetic nystagmus are related to the development of symptoms of motion sickness and gastric tachyarrhythmia.
Abstract: Purpose: The present study investigated the relationship of the frequency of nystagmus to the severity of optokinetic rotation-induced motion sickness. Methods and Results: Eighty-seven subjects viewed a vertically striped, rotating drum for 16 min. Subjects' electrooculograms, ratings of vection, and subjective symptoms of motion sickness (SSMS) were measured during the drum rotation period. Subjects' electrogastrograms (EGGs) were recorded throughout the baseline and drum rotation periods. The ratios of the spectral intensity of EGG 4-9 cycles per minute (cpm) between drum rotation and baseline periods were calculated. The results indicated that the frequency of nystagmus was positively correlated with the ratings of vection (r = 0.40, p < 0.0001), ), scores of SSMS (r = 0.61, p < 0.0001), and ratios of EGG 4-9 cpm spectral intensity between drum rotation and baseline periods (r = 0.54, p < 0.0001). Conclusion: These results demonstrated that more rapid eye movement indexed by higher frequency of optokinetic nystagmus are related to the development of symptoms of motion sickness and gastric tachyarrhythmia.
TL;DR: The vibration and motion characteristics of a commercial pig transporter were measured and a comparison was made between the incidence of travel sickness in pigs and that expected in humans given the measured vehicle vibration characteristics.
Abstract: Low frequency oscillatory motion (0·05 to 0·5 Hz) experienced in ships and road vehicles is known to cause motion sickness in humans and some predictive models are available. There have been very few studies of the incidence of motion sickness in pigs and none which has attempted to identify the frequencies of motion of transporters which are likely to be implicated. In this study, the vibration and motion characteristics of a commercial pig transporter were measured while seven individually penned 40-kg pigs were transported for short (100 min) journeys and 80-kg pigs penned in groups of 12 or 13 were transported for longer (4·5 h) journeys. Direct behavioural observations were made of individual pigs for symptoms of travel sickness (sniffing, foaming at the mouth, chomping, and retching or vomiting). A comparison was then made between the incidence of travel sickness in pigs and that expected in humans given the measured vehicle vibration characteristics. The low frequencies of motion measured on the transporter (0·01 to 0·2 Hz) were well within the range implicated in human motion sickness with considerable power in the longitudinal and lateral axes but little in the vertical axis. On both short and long journeys pigs exhibited symptoms of travel sickness. The likely incidence of travel sickness on the short journeys predicted by the human model was 24 to 31% which corresponds to approximately two of the seven 40-kg pigs becoming travel sick. The numbers observed were generally lower than this although the same pigs were transported twice each day for 2 days and this may have therefore reflected the effects of habituation. The incidence of travel sickness on the long journeys predicted by the human model was 34%. During these journeys which involved four groups of 80-kg pigs which were not repeatedly transported, 26% of pigs vomited or retched (13 out of 50) while 50% showed advanced symptoms of foaming and chomping. These results are not inconsistent with the human model which should form the basis offurther research.
TL;DR: It is hypothesized that central vestibular integration (velocity storage mechanism), by increasing low frequency Vestibular inputs, would favour MS, and found a positive correlation between MS susceptibility and TC.
Abstract: Since motion sickness (MS) never occurs in individuals who lack functional vestibular apparatus, it has been suggested that MS susceptible individuals have more sensitive vestibular systems than non-susceptible people. However, previous investigations involving only stimulation of the semi-circular canals have been inconclusive. We measured gain and time constant (TC) of horizontal canal-ocular reflex (COR) and magnitude of otolith-ocular reflex (OOR). We found that MS susceptibility was not correlated to COR gain but was negatively correlated to OOR magnitude. Thus, MS susceptible individuals do not have more sensitive vestibular systems. We also found a positive correlation between MS susceptibility and TC. We hypothesize that central vestibular integration (velocity storage mechanism), by increasing low frequency vestibular inputs, would favour MS.
TL;DR: The results are consistent with a broad spectrum of antiemetic efficacy with at least a part of its action in the early to middle portions of the final common pathway for vomiting.
TL;DR: The WFVR could become a useful terrestrial model of space motion sickness (SMS) because it duplicates the nature of the gravity-dependent sensory conflicts created by microgravity (visual and otolith inputs conflict while somatosensory gravity cues are minimized), and it also duplicates that of the provocative stimulus more closely than any other proposed terrestrial SMS model.
Abstract: We evaluated a new model of motion sickness--an enclosure decorated with visual cues to upright which was immersed either inverted or "front"-wall down, in Johnson Space Center's Weightless Environment Training Facility (WETF) pool. This "WETF False Vertical Room" (WFVR) was tested with 19 male and 3 female SCUBA diver subjects, aged 23 to 57, who alternately set clocks mounted near the room's 8 corners and made exaggerated pitch head movements. We found that (1) the WFVR test runs produced motion sickness symptoms in 56% and 36% of subjects in the room-inverted and room-front-down positions, respectively. (2) Pitch head movements were the most provocative acts, followed closely by setting the clocks--particularly when a clock face filled the visual field. (3) When measured with a self-ranking questionnaire, terrestrial motion sickness susceptibility correlated strongly (P < 0.005) with WFVR sickness susceptibility. (4) Standing instability, measured with a modified Fregly-Graybiel floor battery, also correlated strongly (P < 0.005) with WFVR sickness susceptibility. This result may reflect a relationship between visual dominance and WFVR sickness. (5) A control study demonstrated that the inverted and front-down positions produced WFVR sickness, but the upright position did not, and that adaptation may have occurred in some subjects with repeated exposure. The WFVR could become a useful terrestrial model of space motion sickness (SMS) because it duplicates the nature of the gravity-dependent sensory conflicts created by microgravity (visual and otolith inputs conflict while somatosensory gravity cues are minimized), and it also duplicates the nature of the provocative stimulus (sensory environment "rule change" versus application of motion to passive subject) more closely than any other proposed terrestrial SMS model. Also, unlike any other proposed terrestrial SMS model, the WFVR incorporates whole-body movement in all three spatial dimensions. However, the WFVR's sensory environment differs from that created by spaceflight in several respects, including the presence of frictional drag on limb movement, magnification at the face-mask-water interface, greater otolith conflict, exhaled bubbles, and the presence of some gravity-dependent somatosensory inputs.
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