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At least 19 recordsLinked to original sources
PubMed1997

Alterations in R-R variability associated with experimental motion sickness.

Motion sickness is a complex integration of responses from multiple physiological systems. Whether the changes that occur during the time course of motion sickness are mediated by the sympathetic or parasympathetic systems is still controversial. The present study evaluates alterations in R-R variability during experimental motion sickness in motion sick and non-motion sick subjects. Ten motion sick subjects and 7 non-motion sick subjects participated in the study. Power spectrum analysis of R-R variation was conducted for all subjects 10 min before a brief vestibular disorientation test (BVDT), for 5-10 min of the test, and 10 min after the test. Subjects were also asked to report their symptoms during the test. The motion sick group showed a significant reduction in the power spectrum density of the R-R interval at the mid and high frequencies during the BVDT test period (BVDT), in comparison with the rest period (Rest). These changes probably indicate a decrease in parasympathetic activity during the time course of motion sickness. The non-motion sick group did not show significant differences at any of the frequencies during BVDT. Power spectrum analysis of the R-R interval provides an objective measure of the autonomic response to experimental motion sickness.

Adolescent↗
PubMed1983

Sensory and motor conflict in motion sickness.

Motion sickness occurs in a wide variety of circumstances involving real or apparent motion, many of them novel and man-made. Significantly, voluntary body movements rarely result in symptoms, and the likelihood of motion sickness is greatly reduced by having control of the vehicle in which one is riding. The unifying theory of Reason [1978] proposes that motion sickness results when there is a mismatch between predicted and actual sensory inputs. Hence, the less predictable the sensory input (because it results from an externally imposed motion, or from motion which results in errors of neural transduction), the more likely that motion sickness will develop. With continuing exposure, predictability increases and adaptation to motion sickness occurs.

Adaptation, Physiological↗
PubMed1985

Endocrine correlates of susceptibility to motion sickness.

Motion sickness releases ACTH, epinephrine, and norepinephrine. We are interested in endocrine responses to motion sickness, in adaptive responses leading to the resolution of the syndrome, and in how antimotion-sickness drugs influence the endocrine responses. Susceptible or insusceptible subjects were administered antimotion-sickness drugs prior to stressful stimulation. Insusceptible subjects displayed more pronounced elevations of ACTH, epinephrine, and norepinephrine after stressful motion. Predrug levels of ACTH were higher in insusceptible subjects (p less than 0.01). Acute blockade of hormone responses to stressful motion or alteration of levels of ACTH by drugs was not correlated with individual susceptibility. No correlation was apparent between epinephrine and ACTH release. These endocrine differences may represent neurochemical markers for susceptibility to motion, stress, or general adaptability, and it may be that the chronic modulation of their levels might be more effective in preventing motion sickness than the acute blockade or stimulation of specific receptors.

Acceleration↗
PubMed2000

Rotation of subjective vertical is an important factor of visually-induced motion sickness.

Motion of visual scene (optokinetic stimulus) projected on a wide screen frequently induces motion sickness. Rotational movements of 3D visual images were analyzed to examine what factors are effective in visually-induced motion sickness and how the gravity contributes to its inducement. While an angle of a rotational axis of 3D visual image from the gravitational direction and its angle from the subjective vertical which was perceived by viewers through 3D visual image were varied, the severity of visually-induced motion sickness was measured.

Adult↗
PubMed1996

Motion sickness.

Motion sickness is a common phenomenon affecting most patients at some point in life. Car sickness, airsickness, seasickness, and space sickness all involve a neural mismatch or confusion between the vestibular, visual, and proprioceptive systems that produces the symptoms of motion sickness. Therapy is directed toward decreasing conflicting sensory input, controlling nausea, and speeding the process of adaptation.

Buspirone↗
PubMed1984

Motion sickness.

Motion sickness affects approximately 90 percent of the population at some time during life, and for many the problem is recurrent and severe. Labyrinthine-defective individuals are "immune." Adaptation is highly specific to one type of motion. Recent studies have focused on the role of the limbic system in mechanisms of motion sickness. Medications are sometimes useful, but they have a high incidence of side effects. Oral agents are ineffective after symptoms develop.

Adaptation, Physiological↗
PubMed1983

Physiological and psychological correlates of motion sickness.

Motion sickness (MS)has been inconclusively associated with personality and physical vestibular functioning in both males and females. The present work consisted of six tests: test of field dependency; pure balance test; motion sickness questionnaire; body steadiness test; primary suggestibility test; resistance to disturbance test. In addition the EPI was completed by a proportion of subjects. Male and female data for the 15 male and 15 female subjects in an age range 20 to 30 years, obtained from within Bedford College, University of London, were factor analysed separately. The results show that, firstly, field dependence, as understood by Witkin, is not associated with any of the factor and correlated significantly (r = 0.83, P less than 0.001; two-tailed test). The same correlation in women was not significantly (r = 0.17). For females, MS and neuroticism appeared on the same factor and correlated significantly (r = 0.62, P less than 0.05; two tailed test). The same correlation in men was not significant (r = 0.06). This suggests that MS in females is associated primarily with neuroticism, whereas in males it is associated with vestibular disturbance thresholds.

Adult↗
PubMed1997

[Motion sickness].

Motion sickness is a general term covering sea-sickness, car-sickness, air-sickness, and space-sickness. Symptoms can occur when a person is exposed to unfamiliar movement whether real or simulated. Despite progress in the technology and comfort of modern transportation (planes, boats, and overland vehicles), a great number of travelers still experience motion sickness. Bouts are characterized by an initial phase of mild discomfort followed by neurologic and gastro-intestinal manifestations. The delay in onset depends on specific circumstances and individual susceptibility. Attacks are precipitated by conflicting sensory, visual, and vestibular signals but the underlying mechanism is unclear. Most medications used for prevention and treatment (e.g. anticholinergics and antihistamines) induce unwanted sedation. Furthermore no one drug is completely effective or preventive under all conditions.

Cholinergic Antagonists↗
PubMed1995

Central cholinergic and alpha-adrenergic mediation of gastric slow wave dysrhythmias evoked during motion sickness.

Motion sickness is associated with gastric slow wave disruption. Animal models of slow wave disturbances show dependence on neural and prostaglandin pathways. Roles of these pathways in circular vection-evoked gastric dysrhythmias and nausea were tested. Eight volunteers with histories of motion sickness underwent vection (60 degrees/s), during which nausea (0 = none to 3 = severe) and electrogastrographic parameters were assessed. Tachygastric activity was expressed as the signal percentage at frequencies of > 4.5 cycles/min. Circular vection induced a maximal nausea score of 2.8 +/- 0 at 513 +/- 66 s. Tachygastric activity increased from 18 +/- 2 to 37 +/- 4% (P < 0.05) and peaked before maximal nausea. Atropine reduced nausea scores to 0 +/- 0 (P < 0.01) with no increase in tachygastric activity (14 +/- 6%). In contrast, the peripheral muscarinic antagonist methscopolamine did not reduce tachygastric activity (46 +/- 4%), nausea (1.8 +/- 0.5), or time to maximal tachygastric activity (504 +/- 80 s) with vection. Phentolamine reduced nausea (1.5 +/- 0.3, P < 0.01) and tachygastric activity, and delayed their onset, whereas propranolol and naloxone had no effect. Pretreatment with oral indomethacin (50 mg) three times daily for 3 days had no effect on vection-evoked tachygastric activity or nausea. To conclude, circular vection evokes gastric dysrhythmias that correlate temporally with maximal nausea and are suppressed by atropine, but not methscopolamine, and are reduced by phentolamine. In contrast to other models of slow wave disruption, endogenous prostaglandins play no role. Thus central cholinergic pathways mediate vection-evoked dysrhythmias with additional modulation by alpha-adrenergic pathways.

Adult↗
PubMed1988

Effects of anti-motion sickness drugs on motion sickness in rats.

Pica, the eating of nonnutritive substances such as kaolin, can be induced by rotation in rats. We used this rotation-induced pica as a behavioral index of motion sickness in rats and examined whether diphenhydramine, methamphetamine and scopolamine, which are anti-motion sickness drugs for humans, are effective for reducing motion sickness in rats. Intraperitoneal injection of diphenhydramine or methamphetamine suppressed the rotation-induced kaolin intake of rats. Intraperitoneal injection of scopolamine had no effect on the rotation-induced kaolin intake, but its transdermal administration reduced this kaolin intake. These findings show that human anti-motion sickness drugs also prevent motion sickness in rats. Since the pharmacological mechanisms for preventing motion sickness in rats and humans are similar, we conclude that rats are a suitable animal model for use in studies on putative anti-motion sickness drugs.

Animals↗
PubMedDate not supplied

Transdermal scopolamine in motion sickness.

Motion sickness is a common clinical malady. Until recently, the use of scopolamine, the drug of choice for the treatment of motion-induced nausea and vomiting, has been sometimes associated with a variety of unacceptable side effects. These side effects could result from the unpredictable blood levels attained with oral dosage (pulse delivery). A new system of drug delivery, the transdermal therapeutic system (TTS)--Transderm-V--has been developed. The TTS delivers scopolamine across the skin at a constant rate. This permits a drug with a very short half life to be administered over prolonged periods, thereby maintaining blood concentrations at the defined therapeutic level. This precludes the necessity for frequent dosing and increases patient acceptability and compliance while minimizing the untoward effects associated with conventional dosage forms of the drug.

Administration, Topical↗
PubMed1997

Psychophysiological aspects of motion sickness.

Motion sickness may occur during travel by sea, automobile, airplane, and space. Susceptibility changes with age and may be influenced by psychological factors. Susceptibility can be reduced in most people by medications that involve histamine or neurotransmitters acetylcholine and noradrenaline, and influence the vestibular system.

Administration, Cutaneous↗
PubMed1987

Head movements in low and high gravitoinertial force environments elicit motion sickness: implications for space motion sickness.

Astronauts report that head movements in flight tend to bring on symptoms of space motion sickness (SMS). We evaluated how head movements in pitch, yaw, and roll--made both with normal vision and eyes-occluded--affect susceptibility to motion sickness in the zero G phase of parabolic flight maneuvers. The findings are clearcut: pitch head movements are most provocative, yaw least provocative, and roll intermediate. Susceptibility is greater with normal vision than with eyes occluded. The same susceptibility pattern emerged for head movements in the 1.8-2.0 G phase of parabolic flight. These experiments suggest that SMS is not a unique nosological entity but, rather, is the consequence of exposure to nonterrestrial force levels. Head movements during departures in either direction from 1 G elicit symptoms. This implies that, rather than speaking of "space motion sickness," it would be more appropriate to think in terms of "nonterrestrial motion sickness."

Gravitation↗
PubMed1986

Head movements in non-terrestrial force environments elicit motion sickness: implications for the etiology of space motion sickness.

Space motion sickness has become an operational concern in manned space flight. Considerable evidence exists that head movements in free fall, especially pitch movements, are provocative until adaptation occurs (3,4,8,9,11,17,18,22,26). The question arises whether space motion sickness is an unique nosological entity or is due to body movements in a nonterrestrial force environment, a force environment for which the body's dynamic sensory-motor adaptions to 1 G are no longer appropriate (14,16,18-21). To evaluate this issue, we had subjects make controlled head movements during exposure to high gravitoinertial force levels, 1.8-2.0 G, in parabolic flight maneuvers. Head movements in pitch with eyes open were most evocative of motion sickness, yaw movements with eyes covered were least provocative. This pattern is identical to that which occurs when the same types of head movements are made in the free fall phase of parabolic maneuvers (17,18). It appears that space motion sickness is the consequence of prolonged exposure to a non-terrestrial force background rather than of exposure to free fall per se.

Adult↗
PubMed1991

Why is the driver rarely motion sick? The role of controllability in motion sickness.

The central hypothesis of the work is that the dimension of control-no control plays an important role in motion sickness. Although it is generally agreed that having control over a moving vehicle greatly reduces the likelihood of motion sickness, few studies have addressed this issue directly, and the theoretical explanation for this phenomenon is not completely clear. In this study, we equated groups differing in controllability for head movement, vision, activity, and predictability, which have often been suggested in the literature as explanations for the driver's immunity to motion sickness. Twenty-two pairs of yoked subjects were exposed to nauseogenic rotation. One subject of each pair had control over the rotation and head movements, while the other was exposed passively to the same motion stimulus. Subjects who had control reported significantly fewer motion sickness symptoms and less of a decrement in their well-being, as compared to the yoked subject without control. The results are discussed in relation to Reason's sensory rearrangement theory and the concept of feed-forward mechanisms in motion perception.

Adult↗
PubMed2000

Autogenic-feedback training exercise is superior to promethazine for control of motion sickness symptoms.

Motion sickness symptoms affect approximately 50% of the crew during space travel and are commonly treated with intramuscular injections of promethazine. The purpose of this paper is to compare the effectiveness of three treatments for motion sickness: intramuscular injections (i.m.) of promethazine, a physiological training method (autogenic-feedback training exercise [AFTE]), and a no-treatment control. An earlier study tested the effects of promethazine on cognitive and psychomotor performance and motion sickness tolerance in a rotating chair. For the present paper, motion sickness tolerance, symptom reports, and physiological responses of these subjects were compared to matched subjects selected from an existing database who received either AFTE or no treatment. Three groups of 11 men, between the ages of 33 and 40 years, were matched on the number of rotations tolerated during their initial rotating-chair motion sickness test. The motion sickness test procedures and the 7-day interval between tests were the same for all subjects. The drug group was tested under four treatment conditions: baseline (no injections), a 25 mg dose of promethazine, a 50 mg dose of promethazine, and a placebo of sterile saline. AFTE subjects were given four 30-minute AFTE sessions before their second, third, and fourth motion sickness tests (6 hours total). The no-treatment control subjects were only given the four rotating-chair tests. Motion sickness tolerance was significantly increased after 4 hours of AFTE when compared to either 25 mg (p < 0.00003) or 50 mg (p < 0.00001) of promethazine. The control and promethazine groups did not differ. AFTE subjects reported fewer or no symptoms at higher rotational velocities than subjects in the control or promethazine groups. The primary physiological effect of promethazine was an inhibition of skin conductance level. The AFTE group showed significantly less heart rate and skin conductance variability during motion sickness tests administered after training.

Adult↗