Tactics for Treating Motion Sickness
While motion sickness is very rare during the first two years of life, incidence increases gradually from age 2 through age 12, then begins to decline from that point. Thus, quite frequently, children suffer from the condition during long family trips by car and eventually, in a sense, grow out of it. Nevertheless, in many people it persists, particularly if provoked by any of several risk factors.
Studies have revealed that people who suffer from migraines tend to have a lower motion sickness threshold compared to those who suffer from tension headaches. Simply being female is a factor as well; females are twice as likely as males to develop motion sickness. While the reason for this is not known, it is thought to be related to hormonal changes connected with the menstrual cycle. Similar mechanisms may be involved causing increased susceptibility to motion sickness in women who take oral contraceptives. Stress and anxiety are associated with increased risk a well. During an anxiety episode, hyperventilation, if it occurs, causes respiratory alkalosis (high pH in the body tissues to accelerated removal of carbon dioxide) which seems to contribute as well. Other factors that can contribute to the condition include hot or otherwise uncomfortable environments (such as might occur in a crowded car if returning from college with friends) and dehydration.
There are several treatment tactics available for motion sickness, categorized based on which type of cell receptor the treatment blocks or stimulates. Although the commonly used anti-motion sickness drug, promethazine, acts primarily by way of histamine H1 antagonist properties, it is weakly antidopaminergic as well as strongly anticholinergic and may be used in children older than 2 years of age, albeit with extreme caution. Scopolamine which also is anti-cholinergic may be used as well, though also with caution due to its "belladonna", (Italian for beautiful woman) effects if used in high doses. This refers to effects that result from ingestion of the plant Atropa belladonna, the original source of the drug atropine. The name is connected with the Greek goddess, Atropos, and plant has been used as a medicine and a poison and also to enhance beauty, in a sense, as it dilates pupils. While this was considered beautiful in antiquity, the effects also include increased sensitivity to light (photophobia) and blurred vision, along with headache, dry mouth, urinary retention and constipation, confusion, tachycardia (rapid heart rate), hallucinations, convulsions, and various other undesirable effects.
Since scopolamine is a sedative, as a motion sickness drug in adults it is used with the sympathomimetic dextroamphetamine, but this is contraindicated in children. Promethazine, along with other H1 antihistamines such as cinnarizine, cyclizine, dimenhydrinate, and diphenhydramine work by antagonizing H1 receptors in the brain's vomit center. It is because they penetrate the blood-brain barrier that they are effective, but for the same reason they also produce sedation. In contrast, nonsedating antihistamines do not penetrate the blood-brain barrier. Consequently, while they are extremely useful in treating allergic rhinitis, they have no effect on the brain's vomit center, and thus are not appropriate treatment for motion sickness.
For centuries, ginger (Zingiber officinalis) has been used as a treatment for motion sickness. Some studies comparing ginger with a placebo have suggested that it actually does work at a dose of 1 to 2 grams, though other studies have suggested that the effects are inconsistent. Thus, as a countermeasure to motion sickness, many people found that eating ginger snaps works well for them. According to a study comparing ginger with dimenhydrinate, the mechanism of action for the effect has nothing to do with direct effects on the central nervous system or the autonomic nervous system. Instead, mechanism of action appears to be linked with effects on gastric motility.