Abstract

While often effective, drug remedies for motion sickness typically induce undesirable side effects. Ondansetron has been explored as an alternative due to its proven prophylactic effect on the vomiting associated with chemotherapy and relative lack of side effects. Previous research indicates that ondansetron may inhibit tachyarrhythmia, a pattern of stomach electrical activity associated with nausea and motion sickness, which may in turn help prevent the development of some motion sickness symptoms. Sixty‐three participants with positive history of motion sickness and self‐treatment of motion sickness were selected. Participants were divided into three groups: placebo, 100 mg dimenhydrinate, and 24 mg ondansetron. Participants were given one of the three treatments 1 hour before exposure to a rotating chair stimulus. Electrogastrograms were measured during a 20‐min baseline and while participants were rotated in complete darkness for up to 20 minutes at 20 rpm while making timed head movements. There were no statistically significant differences between dimenhydrinate, ondansetron, or placebo in the number of head movements tolerated, the amount of time tolerated in the rotating chair, or on subjective motion sickness symptoms. All groups showed a marginally significant decrease in normal three cycles per minute (cpm) activity (F (1/45) = 3.04, p < 0.10) and a significant increase in gastric tachyarrhythmia (F (1/45) = 9.71, p < 0.05). There were no significant differences between the groups and no significant interactions of time (baseline vs. rotation) found in the electrogastrogram data. There were no statistically significant correlations with subjective symptom measures. 3 cpm activity during baseline was positively correlated with rotation duration (r = 0.31) and number of head movements tolerated (r = 0.311), meaning that baseline levels of 3 cpm activity are somewhat predictive of rotation and head movement toleration. This study revealed that ondansetron is not an effective remedy for motion sickness for highly susceptible people. The findings that ondansetron did not affect the GI measures is in direct contrast with previous findings that suggest ondansetron may inhibit tachyarrhythmia (Levine et al., 2000). This study also provides evidence that dimenhydrinate may not be effective for reducing motion sickness in highly susceptible individuals. From both a subjective and objective perspective, all groups developed motion sickness; not even the “gold standard” dimenhydrinate treatment was effective. It appears there is a group of motion sickness sufferers who lack the adequate treatment they need.

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