Motion sickness--vestibular habituation with the centrifuge.

Nel O, Swart JG, van der Laan FL.

Department of Otorhinolaryngology, University of Pretoria.

People who are prone to motion sickness have a directional preponderance of nystagmus to the left. Centrifuging will change this preponderance to the right in most people, and at the same time reduce their tendency towards motion sickness but only with regard to air travel.

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The stability of individual patterns of autonomic responses to motion sickness stimulation.

Cowings PS, Naifeh KH, Toscano WB.

NASA-Ames Research Center, Moffett Field, CA 94035.

As part of a program to develop a treatment for motion sickness based on self-regulation of autonomic nervous system (ANS) activity, this study examined the stability of an individual's pattern of ANS responses to motion sickness stimulation on repeated occasions. Motion sickness symptoms were induced in 58 people during 2 rotating chair tests. Physiological responses measured were heart rate, finger pulse volume, respiration rate, and skin conductance. Using standard scores, we examined stability of responses of specific magnitudes across both tests. Correlational analyses, analysis of variance, and a components of variance analysis all revealed marked, but quite stable, individual differences in ANS responses to both mild and severe motion sickness. These findings confirm our prior observation that people are sufficiently unique in their ANS responses to motion sickness provocation to make it necessary to individually tailor self-regulation training. Further, these data support our contention that individual ANS patterns are sufficiently consistent from test to test so as to serve as an objective indicator of individual motion sickness malaise levels.

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Motion sickness incidence during a round-the-world yacht race.

Turner M, Griffin MJ.

Human Factors Research Unit, University of Southampton, England.

Motion sickness experiences were obtained from participants in a 9 month, round the world yacht race. Race participants completed questionnaires on their motion sickness experience 1 week prior to the start of the race, during the race, and following the race. Yacht headings, sea states, and wind directions were recorded throughout the race. Illness and the occurrence of vomiting were related to the duration at sea and yacht encounter directions relative to the prevailing wind. Individual crewmember characteristics, the use of anti-motion sickness drugs, activity while at sea, and after-effects of yacht motion were also examined with respect to sickness occurrence. Sickness was greatest among females and younger crewmembers, and among crewmembers who used anti-motion sickness drugs. Sickness varied as a function of drug type and activity while at sea. Crewmembers who reported after-effects of yacht motion also reported greater sickness while at sea. The primary determinants of motion sickness were the duration of time spent at sea and yacht encounter direction to the prevailing wind.

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Effects of histamine and betahistine on rat medial vestibular nucleus neurones: possible mechanism of action of anti-histaminergic drugs in vertigo and motion sickness.

Wang JJ, Dutia MB.

Department of Physiology, Medical School, Edinburgh, UK.

The tonic discharge of 71 medial vestibular nucleus (MVN) neurones was recorded in slices of the dorsal brainstem of young adult rats. Bath application of histamine caused a dose-related excitation in 59 of the 71 cells (83%), the remaining 12 (17%) being unresponsive. Dimaprit, a selective H2 agonist, also caused excitation in all 20 cells tested. The histamine-induced excitation and the response to dimaprit were antagonised by the selective H2 antagonist ranitidine, confirming that the H2 subtype of histamine receptor is involved in mediating the effects of histamine on these cells. Triprolidine, a selective H1 antagonist, also antagonised the excitation caused by histamine, at a concentration (0.3 microM) which left the H2 receptor-mediated response to dimaprit unchanged. Thus the excitatory effects of histamine on MVN cells in the rat involve two components mediated through H1 and H2 receptor-linked mechanisms, respectively. Betahistine, a weak H1 agonist and H3 antagonist, had little excitatory action when applied on its own, but significantly reduced the excitation caused by histamine when the two drugs were applied together. The effects of betahistine were consistent with a partial-agonist action at H1 receptors on MVN cells, reducing the excitatory responses to histamine presumably by occupying these receptor sites in competition with the exogenously applied neurotransmitter. This partial-agonist action of betahistine may be an important part of its mechanism of action in the symptomatic treatment of vertigo and motion sickness, since it is likely to occur not only in the MVN but also in many brain regions, including the thalamus and cortex, which express H1 receptors and which are innervated by the hypothalamic histaminergic system. Thus the effectiveness of betahistine and other anti-H1 drugs against motion sickness may be explained by their action in reducing the effects of the excess histamine release induced in such conditions in various brain areas, including the MVN.

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Teleology of motion sickness.

Takahashi M, Ogata M, Miura M.

Department of Otolaryngology, Yamaguchi University School of Medicine, Japan.

We investigated motion sickness evoked by walking while wearing horizontally reversing goggles. The subjects were 36 healthy adults and 90 children aged 4 to 15 years. Most adults soon displayed not only severe sickness, but also dizziness and instability. Instability was certified by Graybiel's ataxia tests in 10 adults. Young children aged 4 to 5 years rarely became sick; however, they showed marked ataxia manifested as drunken gait, falling, or failure to stand up. In older children, autonomic nervous symptoms became manifest and more severe, but ataxia became less severe since locomotion was stopped by uncomfortable symptoms. The present study strongly suggests that motion sickness makes animals learn loss of spatial orientation, which inevitably produces loss of balance.

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The effectiveness of a motion sickness counselling programme.

Dobie TG, May JG.

Department of Physiology, University of Leeds, UK.

Unselected volunteers were offered a course of instruction in using the cognitive-behavioural approach to helping individuals tolerate the deleterious effects of different motion environments. In order to evaluate that programme, 11 of the participants volunteered to counsel independently individuals who were prone to motion sickness, using cognitive-behavioural training which included reinforcement by visually induced apparent motion. The subjects were pre- and post-tested by an independent observer using tolerance and motion response as the dependent variables. These test scores were compared to previous data obtained with subjects who had received counselling from an experienced counsellor, or had received no such counselling. The results indicated that the newly trained counsellors' subjects showed significant pre- to post-test tolerance to the motion stimulus, although they did not benefit as much as subjects trained by the experienced counsellor. However, in terms of post-test symptomatology and magnitude estimates of motion sickness, the trainees' subjects exhibited as much benefit as did those of the experienced counsellor. These data are taken as strong support for the feasibility of training counsellors to employ this method of alleviating motion sickness.

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Reliability of psychophysiological responses across multiple motion sickness stimulation tests.

Stout CS, Toscano WB, Cowings PS.

NASA-Ames Research Center, Moffett Field, California.

Although there is general agreement that a high degree of variability exists between subjects in their autonomic nervous system responses to motion sickness stimulation, very little evidence exists that examines the reproducibility of autonomic responses within subjects during motion sickness stimulation. Our objectives were to examine the reliability of autonomic responses and symptom levels across five testing occasions using the (1) final minute of testing, (2) change in autonomic response and the change in symptom level, and (3) strength of the relationship between the change in symptom level and the change in autonomic responses across the entire motion sickness test. The results indicate that, based on the final minute of testing, the autonomic responses of heart rate, blood volume pulse, and respiration rate are moderately stable across multiple tests. Changes in heart rate, blood volume pulse, respiration rate, and symptoms throughout the test duration are less stable across the tests. Finally, autonomic responses and symptom levels are significantly related across the entire motion sickness test.

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

Hasler WL, Kim MS, Chey WD, Stevenson V, Stein B, Owyang C.

Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor 48109-0362, USA.

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.

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