Visual field effects on motion sickness in cars.

Griffin MJ, Newman MM.

Human Factors Research Unit, Institute of Sound and Vibration Research, University of Southampton, Southampton, England. M.J.Griffin soton.ac.uk

BACKGROUND: It is commonly assumed that car passengers who suffer from motion sickness will benefit from being able to see the road ahead. Hypothesis: It was hypothesized that variations in the external view (including restrictions to forward view and the provision of an artificial real-time video view) would affect the development of sickness during a 30-min suburban car journey. METHOD: Motion sickness was investigated in 4 experiments using 15 different conditions, with 20 subjects in each condition. The conditions involved artificial restrictions to view, restrictions arising from different seating positions, and the provision of a video view of the road ahead. Subjects provided ratings of motion sickness at 1-min intervals during the 30-min journey. The motion sickness susceptibility of subjects was matched between groups of subjects and the car motions were measured in three axes to determine whether the motion conditions were similar across conditions within each experiment. RESULTS: Absence of a visual field (blindfolded) resulted in similar sickness to that with no external forward view (with or without a side view). A wide or narrow forward view (with or without a side view) reduced sickness. For the conditions of these experiments, seating position did not significantly affect sickness. The provision of a real-time video view of the road ahead did not reduce motion sickness. There was circumstantial evidence that horizontal acceleration at frequencies below 0.1 Hz contributed to sickness. CONCLUSIONS: It is concluded that sickness in cars is dependent on the visual scene. The minimization of sickness by the provision of visual information requires improved understanding of those factors that combine to cause and suppress sickness.

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Factors influencing the susceptibility of anurans to motion sickness.

Naitoh T, Wassersug RJ, Yamashita N.

Department of Biological Science, Shimane University, Matsue 690-8504, Japan. naitoh-t life.shimane-u.ac.jp

We examined the propensity for motion sickness in five anuran species, concentrating our efforts on the treefrog Rhacophorus schlegelii, because it had shown the greatest susceptibility to motion sickness in a previous study. We used parabolic flight as our provocative stimulus and fed all specimens a known volume of food 1.5-3 h before flight. The presence of vomitus in a frog's cage was our indicator of motion sickness. Significantly more emesis was observed in flight-exposed than in control R. schlegelii (P < 0.05). There was no sex difference in susceptibility to motion sickness (P > 0.5). Individuals that vomited were significantly larger (P < 0.02) than those that did not. Among microgravity-treated frogs, those that vomited spent on average 85% more time airborne and tumbling in microgravity than those that did not vomit (P=0.031). Our data support the view that postural instability and sensory conflict are elements of motion sickness in anurans. Specifically, conflicts between tactile, vestibular and visual input seem essential for producing motion-induced emesis in anurans. Since the factors that induce motion sickness in R. schlegelii are the same ones that produce motion sickness in humans, arboreal frogs may be useful alternative models to mammals in motion sickness research.

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Effects of amygdala or hippocampus lesion on hypergravity-induced motion sickness in rats.

Uno A, Takeda N, Horii A, Sakata Y, Yamatodani A, Kubo T.

Department of Otolaryngology, Suita Municipal Hospital, Japan. auno ent.med.osaka-u.ac.jp

We examined the effects of amygdala lesion (AL) or hippocampal lesion (HL) on hypergravity-induced motion sickness in rats. Rats do not vomit, but the behavior known as pica, the eating of non-nutritive substances such as kaolin, can be used as an index of motion sickness. In the present study, hypergravity-induced kaolin intake and apomorphine-induced kaolin intake were measured before and after brain lesions. After AL, hypergravity-induced kaolin intake and the ratio of the hypergravity- to apomorphine-induced kaolin intakes were decreased. These results indicate that AL suppressed motion sickness more than pica behavior itself, suggesting that the amygdala plays an important role in the development of motion sickness in rats. Conversely, after HL, hypergravity-induced kaolin intake was increased, as was the ratio of the hypergravity- to apomorphine-induced kaolin intakes. These results indicate that HL aggravates motion sickness induced by hypergravity in rats, suggesting that the hippocampus counteracts motion sickness.

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Motion sickness.

Golding JF, Gresty MA.

Department of Psychology, University of Westminster, London, UK.

PURPOSE OF REVIEW: The public's longstanding resigned tolerance to motion sickness threatens to change, due to the widespread introduction of nauseogenic tilting trains and the increasing use of virtual reality immersion. RECENT FINDINGS: Scientific effort over the last 5 years has focused on precise evaluation of the stimuli that provoke sickness and on the development of behavioural and new pharmacological interventions to suppress sickness. SUMMARY: The precise mechanical ride characteristics of vehicles that provoke sickness have been identified and this will lead to guidelines for future engineering design, especially for suspension systems that compensate for inertial tilt, and recommendations for passengers at risk. The frequency characteristics of motion provoking sickness have been defined with greater precision and identified with shifts in perception of motion versus orientation, and changes in the quality of reflex eye movements. Ability to modify readily the time constant of vestibular 'velocity store' has emerged as a potential candidate marker of successful motion sickness habituation. Behavioural 'autogenic' countermeasures to the development of sickness, such as controlled breathing, which can be implemented readily, are shown to have significant ameliorating effects on nausea and are of value for short term moderate exposures. New classes of pharmacological agents such as N-methyl-D-aspartate antagonists and 5HT1a receptor agonists show promise in animals but await trials in humans.

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Motion sickness: its pathophysiology and treatment.

Sakata E, Ohtsu K, Sakata H.

Center for Vertigo, Disequilibrium, and Tinnitus Diseases, Tokyo, Japan.

The pathogenesis of motion sickness includes both inner-ear stimulation by body movement, especially a Coriolis-type stimulus, and optokinetic stimulation due to the shift of the surrounding visual fields. According to Kornhuber, Sakata and others, the vestibular cerebellum also participates in an important way. We conducted this study to elucidate the influence of the vestibular cerebellum on the development of motion sickness. We initially focused attention on the visual suppression test of Takemori et al. as a test for vestibular cerebellar function. We reported a modification of this test, described as postrotatoric nystagmus. We employed this test as a rotatoric visual suppression test using milder stimulus for patients complaining of motion sickness. The pathogenesis and treatment of motion sickness are also discussed.

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Cerebral hypoperfusion precedes nausea during centrifugation.

Serrador JM, Schlegel TT, Black FO, Wood SJ.

Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. serrador hms.harvard.edu

INTRODUCTION: Nausea and motion sickness are important operational concerns for aviators and astronauts. Understanding the underlying mechanisms associated with motion sickness may lead to new treatments. The goal of this work was to determine if changes in cerebral blood flow precede the development of nausea in subjects susceptible to motion sickness. METHODS: Cerebral flow velocity in the middle cerebral artery (transcranial Doppler), BP, and end-tidal CO2 were measured while subjects were rotated on a centrifuge (250 degrees x s(-1)). Following 5 min of rotation, subjects were translated 51.5 cm off-center, creating a +1 Gx centripetal acceleration in the nasal-occipital plane. RESULTS: There were 10 subjects who completed the protocol without symptoms while 5 developed nausea (4 while off-center and 1 while rotating on-center). Prior to nausea, subjects had significant increases in BP (+13 +/- 3 mmHg, p < 0.05) and cerebrovascular resistance (+46 +/- 17%, p < 0.05) and decreases in cerebral flow velocity both in the second (-13 +/- 4%) and last minute (-22 +/- 5%) before symptoms (p < 0.05). In comparison, subjects resistant to motion sickness demonstrated no change in BP or cerebrovascular resistance in the last minute of off-center rotation and only a 7 +/- 2% decrease in cerebral flow velocity. All subjects had significant hypocapnia (-3.8 +/- 0.4 mmHg, p < 0.05); however, this hypocapnia could not fully explain the cerebral hypoperfusion associated with the development of nausea. CONCULSIONS: These data indicate that reductions in cerebral blood flow precede the development of nausea. Further work is necessary to determine what role cerebral hypoperfusion plays in motion sickness and whether cerebral hypoperfusion can be used to predict the development of nausea in susceptible individuals.

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

Gupta VK.

Dubai Police Medical Services, P.O. Box 12005, Dubai, United Arab Emirates.

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.

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Motion sickness in public road transport: passenger behavior and susceptibility.

Turner M, Griffin MJ.

Department of Psychology, University of Portsmouth, UK.

The aim of this research was to identify personal and environmental factors influencing individual susceptibility to motion sickness during road transport. A questionnaire survey of 3256 coach travellers was conducted. Information on passenger characteristics, travel regularity, activity during travel, use of anti-motion sickness drugs and self-reported motion sickness susceptibility were collected over 56 private hire coach journeys. Details of the travel environment (visibility, temperature and seating) were also recorded. The relationship of these variables with passenger illness and more specific symptoms of motion sickness are examined. Overall, 28.4% of passengers reported feeling ill, 12.8% reported nausea and 1.7% reported vomiting during coach travel. Travel sickness decreased with increasing passenger age and greater travel experience. Females were more likely to report feeling ill during coach travel than males by a ratio of four to three. Poor forward visibility was found to increase sickness. Passenger illness occurrence was approximately three times higher for passengers with no view of the road ahead (mean, 34.6%) compared to passengers who could see the road ahead extremely well (mean, 12.7%). No relationships were found between the occurrence of travel sickness and temperature or time of travel. Differences in the pattern of sickness responses exhibited by coach travellers suggest: (1) habituation through greater travel regularity may occur independently of reductions in travel sickness that occur with age; (2) females are more affected by poor forward visibility than males; and (3) the incidence of travel sickness could be significantly reduced by improving the external visibility afforded to passengers.

Online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10048305&dopt=Abstract motion sickness