Prophylactic effect of serotonin uptake inhibitors against motion sickness in Suncus murinus.

Okada F, Saito H, Matsuki N.

Department of Chemical Pharmacology, Faculty of Pharmaceutical Science, University of Tokyo, Japan.

The prophylactic effect of serotonin uptake inhibitors, imipramine and fluoxetine, against motion sickness was investigated in Suncus murinus. Imipramine (s.c.) and fluoxetine (i.p.) inhibited motion-induced emesis dose dependently with ID50 values of 1.7 and 26 mg/kg, respectively. The results suggest that increasing the concentration of serotonin in the synaptic cleft can prevent motion-induced emesis and that serotonin uptake inhibitors are effective as anti-motion sickness drugs.

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"Torso rotation" experiments; 1: Adaptation to motion sickness does not correlate with changes in VOR gain.

Bouyer LJ, Watt DG.

Aerospace Medical Research Unit, McGill University, Montreal, Canada. bouyer medcor.mcgill.ca

Following a 30-minute exposure to an unusual motor strategy called "Torso Rotation" (TR), the signs and symptoms of motion sickness appear along with perceptual illusions during movement, gaze and postural instability, and a significantly reduced vestibulo-ocular response (VOR) gain. With repeated exposure to TR, the motion sickness disappears and gaze instability seems to be reduced. Is this apparent improvement in gaze stability associated with a reduction of the transient change in VOR gain? Motion sickness (subjective questionnaire) and VOR gain (passive step rotations in darkness) were measured before and repeatedly after TR on 7 consecutive days. Despite a complete loss of symptoms in 3 to 4 days, the transient, daily change in VOR gain remained unaffected. Furthermore, there was no increase in the use of compensatory saccades. It is concluded that adaptation to TR-induced motion sickness is not the result of a change in VOR's sensitivity to TR.

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"Torso rotation" experiments; 2: Gaze stability during voluntary head movements improves with adaptation to motion sickness.

Bouyer LJ, Watt DG.

Aerospace Medical Research Unit, McGill University, Montreal, Canada. bouyer medcor.mcgill.ca

Following a 30-minute exposure to an unusual motor strategy called "Torso Rotation" (TR), the signs and symptoms of motion sickness appear along with perceptual illusions during movement, gaze and postural instability, and a significantly reduced vestibulo-ocular response (VOR) gain. With repeated exposure to TR, motion sickness symptoms disappear and gaze instability seems reduced, but without any concomitant change in VOR gain. Is the reduction in gaze instability a perceptual illusion or a real, measurable phenomenon? Velocity gain (eye velocity/ head velocity) was evaluated during voluntary head shaking in the light over the frequency range 0.3 to 3.0 Hz. A significant improvement was seen after 3 days of testing (P < 0.01). Furthermore, the time course of improvement in gaze stability was correlated with the loss of motion sickness symptoms reported in the previous study (1). We suggest that adaptation to motion sickness could be related to an overall change in sensori-motor strategy, perhaps including a de-emphasis of a vestibular reference.

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A ground-based animal model of space adaptation syndrome.

Takeda N, Horii A, Uno A, Morita M, Mochizuki T, Yamatodani A, Kubo T.

Department of Otolaryngology, Faculty of Medicine, Osaka University, Japan.

We examined the effect and aftereffect of acute or chronic load of hypergravity produced by an animal centrifuge, on pica (that is, kaolin intake) in the rat as an index of motion sickness. Although the degree of pica initially induced by acute or chronic hypergravity was not different, the rate of decline of increased kaolin intake over poststimulus days was different. Pica after a 1-h load of 2g decreased rapidly. On the other hand, pica lasted 3 days after a 48-h load of 2g. These findings suggest that the aftereffects of chronic hypergravity application on pica are due to motion sickness induced by readaptation to normal gravity, and they support our idea that after adaptation to a hypergravity environment, return and readaptation to the normal gravity can simulate exposure and adaptation to microgravity. We concluded that motion sickness in rats induced by the aftereffects of chronic hypergravity stimulation can be used as a ground-based animal model of space adaptation syndrome.

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Effects of spatial frequency of a vertically striped rotating drum on vection-induced motion sickness.

Hu S, Davis MS, Klose AH, Zabinsky EM, Meux SP, Jacobsen HA, Westfall JM, Gruber MB.

Department of Psychology, Humboldt State University, Arcata, CA 95521, USA.

PURPOSE: The present study investigated the effects of differential spatial frequencies of a vertically striped, horizontally rotating drum on the observer's frequency of eye nystagmus, perceived velocity of self-motion, and symptoms of motion sickness. METHODS AND RESULTS: Two experiments were conducted. In Experiment 1, each of 10 subjects viewed 1 min of an optokinetic rotating drum at the speed of 10 rpm covered with 6, 12, 24, 48, and 96 pairs of black and white stripes, presented in counterbalanced order. The results indicated that subjects perceived significantly stronger circular vection (p < 0.05) and generated significantly higher frequencies of eye nystagmus (p < 0.05) when they were viewing 24 pairs of black and white stripes than when they were viewing any of the other combinations of 6, 12, 48, or 96 black and white stripes. In Experiment 2, 100 highly susceptible subjects viewed 16 min of an optokinetic rotating drum covered with one of the five different numbers of black and white stripe pairs: 6, 12, 24, 48, and 96. The results indicated that subjects in the group viewing 24 moving contrasts perceived significantly stronger circular vection (p < 0.001), reported significantly more severe symptoms of motion sickness (p < 0.001), and showed significantly greater ratios of EGG 4-9 cycles per minute spectral intensity between drum rotation and baseline periods (p < 0.004) than those in the groups of viewing 6, or 96 moving contrasts. CONCLUSION: These results demonstrated that the severity of vection-induced motion sickness is affected by differential spatial frequencies of the stripes of the rotating drum and may be affected by number of horizontal eye movements.

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Role of plasma vasopressin as a mediator of nausea and gastric slow wave dysrhythmias in motion sickness.

Kim MS, Chey WD, Owyang C, Hasler WL.

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

The possible role of vasopressin in nausea and gastric dysrhythmias in motion sickness was tested by electrogastrography in 14 subjects during circular vection (60 degrees/s) and vasopressin infusion. Tachygastria was expressed as the signal percent >4.5 cycles/min. Vection evoked nausea scores of 2.6 +/- 0.2 (0 = none to 3 = severe) in 10 subjects with increases in tachygastric activity (15 +/- 2 to 45 +/- 3%) and plasma vasopressin (4.5 +/- 1.5 to 8.4 +/- 2.5 pg/ml) that were blocked by atropine but not indomethacin. Four asymptomatic subjects had no tachygastria or vasopressin release. Vasopressin at 0.2 U/min (plasma level = 322.1 +/- 10.3 pg/ml) evoked nausea (2.6 +/- 0.4) and increases in tachyarrhythmic activity (41 +/- 5%) that were blunted by atropine but not indomethacin. There were no differences in nausea or dysrhythmias with vasopressin infusion in subjects who noted nausea during vection versus those who did not. To conclude, vection evokes nausea, dysrhythmias, and vasopressin release in motion sickness-susceptible humans via cholinergic prostaglandin-independent pathways. Supraphysiological vasopressin infusions evoke nausea and dysrhythmias by similar pathways to equal degrees in motion sickness-susceptible and -resistant subjects. Thus central but not peripheral actions of vasopressin may contribute to nausea and slow wave disruption with vection. Blunting of both the release and action of vasopressin by atropine may explain its beneficial action in motion sickness.

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Frequency effect of 0.35-1.0 Hz horizontal translational oscillation on motion sickness and the somatogravic illusion.

Golding JF, Finch MI, Stott JR.

Centre for Human Sciences, Farnborough, Hants, United Kingdom.

BACKGROUND: Low frequency translational oscillation can provoke motion sickness in land vehicles, ships and aircraft. HYPOTHESIS: Nauseogenicity should decrease towards the higher frequencies. METHODS: Some 12 subjects were exposed to horizontal sinusoidal motion (3.6 m.s-2 peak) at four different frequencies 0.35, 0.50, 0.70, and 1.00 Hz, at 1-week intervals, latin square order. Subjects were seated in the upright position; motion was through the head-body X-axis. Motion was stopped (motion endpoint) at moderate nausea or after 30 min. RESULTS: The proportion of subjects experiencing moderate nausea decreased towards the higher frequency: 9/12 at 0.35 Hz, 3/12 at 0.50 Hz, 0/12 at 0.70 Hz, and 2/12 at 1.00 Hz. The mean time to motion endpoint increased significantly (p < 0.001) towards the higher frequency: 17.4 min 0.35 Hz; 26.0 min 0.50 Hz; 30 min 0.70 Hz; 28.3 min 1.00 Hz. Differences between frequencies were significant (0.001 < p < 0.05) except for 0.70 Hz to 1.00 Hz. At all frequencies tested, horizontal stimuli were more nauseogenic than predicted by mathematical models based on the frequency and intensity of vertical oscillation. Somatogravic illusion (SGI) was reported by 9/12 subjects (mean illusory tilt angles 15.6 degrees forward, 14.1 degrees back). SGI tended to diminish at the higher frequencies, but there was no relationship between SGI and motion sickness. CONCLUSIONS: These results confirm previous findings (9), and furthermore indicate that horizontal X-axis translational oscillation has greatly reduced nauseogenic potential at frequencies greater than 0.5 Hz. A mathematical model is proposed to predict motion sickness intensity and incidence due to this stimulus, which may also be applicable to equivalent Y-axis motion.

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Histamine release from the hypothalamus induced by gravity change in rats and space motion sickness.

Uno A, Takeda N, Horii A, Morita M, Yamamoto Y, Yamatodani A, Kubo T.

Department of Otolaryngology, Faculty of Medicine, Osaka University, Suita, Japan. auno mr-mbio.med.osaka-u.ac.jp

Freely moving rats were exposed to 2 g hypergravity in an animal centrifuge device to produce motion sickness. Histamine release from the anterior hypothalamus of the rats was measured in vivo with a microdialysis technique. After a 2-h load of 2 g hypergravity, rats ate kaolin. Because pica, eating a nonnutritive substance such as kaolin, is a behavioral index of motion sickness in rats, this finding indicates that the rats suffered from motion sickness. During 2 g hypergravity for 2-h, histamine release from the hypothalamus was transiently increased. In contrast, neither the transient increase of histamine release nor the kaolin consumption were induced by 2 g hypergravity in bilaterally labyrinthectomized rats. Pretreatment with alpha-fluoromethylhistidine, an inhibitor of histamine-synthesizing enzyme, decreased both the basal and hypergravity-induced releases of histamine from the hypothalamus and suppressed the kaolin consumption induced by hypergravity. Taken together, these findings suggest that the vestibular information of changes in gravity activate the histaminergic neuron system, resulting in the development of motion sickness. More prolonged stimulation, a 4-h load of 2 g hypergravity, induced significant increase of kaolin consumption on postdays 1-3, though rats ate kaolin on postdays 1-2 after 2 g hypergravity for 2 h. During 2 g hypergravity for 4 h, the initial transient increase of histamine release was followed by the gradual increase of histamine release after the end of centrifugation. It is suggested that rats adapted to the hypergravity environment after centrifugation for 4 h, but not 2 h, so that the change in gravity from 2 g to 1 g became a provocative stimulation. We, therefore, concluded that motion sickness in rats induced by a negative change in gravity can be used as a simulation of space motion sickness, which is induced by exposure to microgravity. Histaminergic activation in the development of motion sickness induced by negative change in gravity might be an underlying mechanism of space motion sickness.

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