A stimulator for laboratory studies of motion sickness in cats.

Crampton GH, Lucot JB.

A motion sickness device is described which produces motion sickness in about 40% of an unselected population of unrestrained female cats during a 30-min exposure at 0.28 Hz. The apparatus provides a gentle wave stimulus, similar to that provided by an amusement park Ferris Wheel. Two cats may be tested at the same time. This device is useful for studies of putative antimotion sickness drugs or the biochemical basis of the emetic response to motion.

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Transderm scopolamine efficacy related to time of application prior to the onset of motion.

Levy GD, Rapaport MH.

We evaluated Transdermal Scopolamine related to the time of application prior to the onset of motion. In this study 44 subjects participated. The first group applied the transdermal disc within 4 h and the second group 8 h or more prior to the onset of motion. We observed a significant decrease in the incidence and the degree of motion sickness for the group with at least 8 h of scopolamine application prior to sea travel. Therefore, the transdermal scopolamine system should be applied at least 8 h before potentially disturbing motion to provide adequate prophylaxis against motion sickness. We found no significant difference in motion sickness susceptibility between men and women, in contrast to earlier reports.

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Serum levels of eleven steroid hormones following motion sickness.

Stalla GK, Doerr HG, Bidlingmaier F, Sippel WG, von Restorff W.

In order to grade motion sickness objectively, the following 11 adrenal hormones were investigated in subjects with different motion sickness susceptibility: Aldosterone, corticosterone, 11-deoxycorticosterone, progesterone, 17-OH-progesterone, 11-deoxycortisol, cortisol, cortisone, testosterone, androstendione, dehydroepiandrosterone sulfate. Motion sickness was induced by the coriolis effect on a rotary chair. Both severe kinetosis after short rotation time and mild motion sickness after 30 min of rotation occurred together with small hormonal changes. Androstendione and 11-deoxycortisol appear to be sensitive indicators of motion sickness if the rotation time is taken into consideration. A significant increase of all hormones except progesterone, cortisone, testosterone, and dehydroepiandrosterone sulfate was observed when pronounced malaise had come after a long rotation stress (24.6 min). The changes in plasma aldosterone concentration appeared to correlate with time only. The present study demonstrates that hormonal analysis can be helpful in estimating the degree of motion sickness.

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Appropriateness of kaolin consumption as an index of motion sickness in the rat.

McCaffrey RJ.

The appropriateness of kaolin consumption, one form of pica, as an index of motion sickness in the rat was examined. Unlike other motion sickness indices, the use of kaolin consumption results in a bitonic function across daily rotation sessions. This bitonic function is not predicted from any theory of motion sickness (viz., the Sensory Rearrangement Theory), rather an inverse relationship should exist between the severity of motion sickness and repeated exposure to the effective motion (i.e., habituation). The results of Experiments 1 and 2 support the continued use of kaolin consumption as an index of motion sickness in the rat. A response interference process is proposed to account for the first portion of the bitonic kaolin consumption function with grooming possibly representing a higher probability behavior than kaolin consumption. Experiment 3 examined and confirmed that kaolin consumption indexes the process of rehabituation to an effective motion. This extends the number of principles that are characteristic of motion sickness exhibited by species capable of emesis and supports the continued use of kaolin consumption as an index of motion sickness and general gastrointestinal malaise in the rat.

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Effects of head and body restraint on experimental motion-induced sickness in squirrel monkeys.

Wilpizeski CR, Lowry LD, Contrucci RB, Green SJ, Goldman WS.

Each of 16 Bolivian-phenotype squirrel monkeys of mixed sex had a machine bolt mounted on the skull with acrylic cement; 13 were provided with temporary plaster body casts allowing free movement. With eyes open, all were rotated in the horizontal plane at 30 rpm every other day until vomiting occurred or for a maximum duration of 120 min/spin. Latencies for motion-sickness signs were recorded under three experimental conditions: free movement, torso fixed to an aluminum frame and both torso and head restrained by bolting to the frame. Subsequently, 10 monkeys from this sample were rotated while blindfolded with head and torso immobilized. Results partially confirmed human and animal findings reported by others: reduced mobility was accompanied by a reduction in the incidence and an increase in the latency of motion sickness. The importance of optokinetic input for the generation of motion sickness in this species was clear.

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Tachygastria and motion sickness.

Stern RM, Koch KL, Leibowitz HW, Lindblad IM, Shupert CL, Stewart WR.

Cutaneously-recorded electrogastrograms (EGGs) were obtained from 21 healthy volunteers who were seated within a drum, the rotation of which produced vection or illusory self-motion. Fourteen subjects developed symptoms of motion sickness during vection and in each the EGG frequency shifted from the normal 3 cpm to 5-8 cpm, tachygastria, an abnormal pattern. In 6 of 7 asymptomatic subjects, the 3 cpm EGG pattern was unchanged during vection. It was concluded that illusory self-motion produces tachygastria and motion sickness in susceptible subjects.

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Evidence for a motion sickness agent in cerebrospinal fluid.

Crampton GH, Daunton NG.

The possibility that there might be a neurohumoral cerebrospinal fluid (CSF) link in motion sickness was directly tested in cats by blocking the flow of CSF from the third into the fourth ventricle. Evidence obtained thus far is consistent with the hypothesis. Cats with demonstrably sound blocks did not vomit in response to an accelerative motion sickness stimulus, whereas cats with imperfect 'leaky' blocks vomited with little or no increase in latency. Although there are several putative candidates, the identification of a humoral motion sickness substance is a matter of conjecture.

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A 1983 neuropharmacologic perspective of space sickness.

Borison HL.

Space sickness is generally considered a variant of motion sickness although not fully proved as such. Understanding space sickness requires objective and quantitative characterization of the disorder. Vomiting is a quantifiable physiological event performed by the respiratory muscles which generate the pressures that evacuate the gut. Vomiting from all causes is coordinated by the vomiting center in the medulla oblongata. The emetic chemoreceptor trigger zone (CTZ) in the area postrema is thought to be an indispensable element in the afferent pathway of motion sickness. About 30 potential neurotransmitters exist in the vomiting control mechanism which includes at least eight chemical transmission steps through the reflex pathway of motion sickness. Individual synaptic transmitters do not likely mediate specific functions, but particular combinations of those transmitters might well serve distinct functions. Adaptation to the cause of space sickness probably results from readjustment of a cerebellar circuit or of a humoral factor acting on the CTZ, rather than from stimulus-receptor desensitization. Space sickness must, for purposes of investigation, be treated as a unique disorder engendered by weightlessness until proved equivalent to any emetic syndrome that occurs on earth.

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