Purpose
Background
"Sailing on the sea proves that motion disorders the body," observed the Greek physician Hippocrates, over 2,000 years ago. The word "nausea" derives from the Greek root word naus, meaning "ship," from which "nautical" is also derived. In modern times, motion sickness can be provoked by a wider range of situations, including cars, buses, trains, aircraft, roller coasters, virtual reality, simulators, and even movement in outer space. People vary in their susceptibility, but given a sufficient stimulus, almost all people with functional vestibular systems (responsible for balance and spatial orientation) can develop motion sickness.
Signs and symptoms
The primary symptoms of motion sickness are nausea and vomiting. Related symptoms (Box 7.6.1) include drowsiness (sometimes termed "sopite syndrome"), gastrointestinal discomfort, increased salivation, sensations of bodily warmth, dizziness, and facial pallor and sweating (so-called cold sweating). The onset of motion sickness is usually gradual, the timescale being determined by the intensity of the stimulus and the susceptibility of the individual. Patterns of symptoms vary but usually progress from initial symptoms, such as stomach awareness, feelings of warmth, yawning, sweating, dizziness, through to nausea and ultimately to vomiting. Compared to real-world experiences, the occurrence of symptoms such as eyestrain and headache is higher in virtual reality systems and simulators.
Box 7.6.1
Mechanisms and theories
The most widely accepted explanation for motion sickness is the sensory conflict or neural mismatch theory. The sensory conflict or mismatch is between incoming patterns of vestibular, visual, and kinesthetic (perception of motion) inputs versus the expected patterns as predicted by an "internal model." For example, when in a ship or other vehicle with limited outside visibility, the vestibular system reports motion to the central nervous system, but information from the visual system suggests the individual is not moving. If inconsistencies in the patterns are detected, centers in the brain are activated that mediate the signs and symptoms of motion sickness. From this perspective, behavioral countermeasures, such as obtaining a horizon view and avoiding visual tasks, are based on reducing visual-vestibular mismatches, whereas habituation, desensitization acquired over multiple exposures, updates the "internal model" to accept new patterns of sensory relationships (Table 7.6.1).
Table 7.6.1: Behavioral countermeasures against motion sickness
| Countermeasure | Comments | Possible Limitations |
|---|---|---|
| Habituation (desensitization) | The most effective countermeasure; fully acquired habituation is more effective than any current anti-motion-sickness drugs and free of side effects | Can be slow to acquire, often stimulus-specific; it may need periodic re-exposure to motion to maintain adaptive protection |
| Obtaining visual horizon reference | Shown to provide some protection in ships, ship simulators, buses, and cars | Often not possible (e.g., if below deck at sea) |
| Avoiding reading or visual scanning | Shown to reduce motion sickness in a variety of transport or simulator environments | Often not compatible with performance of visual tasks such as map reading, monitoring displays, etc. |
| Avoiding head movements | Reduces motion sickness in a variety of transport environments | Often not compatible with effective task performance |
| Lying supine | May be effective by reducing head movements rather than posture per se | Often not compatible with effective performance of most tasks |
| Aligning body with gravito-inertial force vector; i.e., avoiding postural instability by aligning with direction of gravity and any imposed forces | Shown to be effective both in the laboratory and outside: at sea, align the standing posture with the motion of the ship, sometimes called “wave-riding” or getting “sea legs”; as a car passenger, lean into the bends when cornering | Requires experience and some degree of accurate anticipation of motion |
| Avoiding locations of maximum motion | For example, avoid locations such as the bow of a ship; in aircraft, sit near the wings | Often not possible |
| Being in control | For example, being the driver or the pilot; also, there is evidence that perception of “controllability” is important | Not possible as a passenger |
| Systematic controlled breathing | Laboratory trials show this strategy to be around half as effective as anti-motion-sickness drugs; unlike drugs, it is free of side effects | Requires some degree of training; also requires some degree of attention, which may interfere with complex tasks |
Notes
Apart from habituation, other behavioral countermeasures are only partially effective.
Individual susceptibility and risk factors
Children under 2 years of age do not usually experience motion sickness. Susceptibility then rises, peaks between the ages of 7 and 12 years, and later declines through adulthood to old age, perhaps because of habituation. However, susceptibility may increase in a small minority of individuals in old age. Surveys report that women are more susceptible than men, but this is a much smaller effect than age. Hormonal factors, such as the use of oral contraceptives, menstruation, pregnancy, and cortisol levels, correlate with motion sickness susceptibility in women, further complicating any association of female sex with susceptibility. People with a history of migraine, vertigo, or vestibular disorders are more prone to motion sickness. Evidence from twin studies suggests that a large proportion of individual variation in susceptibility is due to genetic factors, with heritability accounting for 55%–70% of the variation; multiple genes may be involved.
Behavioral and other nonpharmacologic countermeasures
Awareness and avoidance of situations that trigger symptoms are primary strategies against motion sickness. Behavioral interventions to prevent motion sickness are summarized in Table 7.6.1. Being sleep-deprived can worsen motion sickness. Alcohol consumption and smoking (nicotine) should be avoided because they increase motion sickness. The efficacy of particular diets, supplements, vitamins, ginger, and so on, has only weak and contradictory supporting evidence. Distractions may be useful, such as getting fresh air on the face, listening to music, and pleasant scents. "Controlled breathing" is concentrating on breathing at a regular pace which is the same as one's normal resting breathing rate. The effect appears more than just simple distraction, perhaps due to activating the reciprocal inhibitory defense reflex between respiration and vomiting. Laboratory trials show that acupressure bands or similar treatments are no more effective than placebo. However, placebo effects can be strong, and if an individual finds they work, they may still be useful. Habituation is the most effective countermeasure—even more than any medication—but can be slow to acquire and may require periodic re-exposure to maintain efficacy.
Pharmacologic countermeasures
Drugs are useful in situations where habituation is impractical, such as single or infrequent journeys. Individuals should be advised that medication is most effective when taken before exposure, rather than after the onset of symptoms. Drugs against motion sickness can be divided into the following categories: antimuscarinics (e.g., scopolamine); H1 antihistamines (e.g., dimenhydrinate); and sympathomimetics (e.g., amphetamine). All effective anti-motion-sickness drugs penetrate the blood-brain barrier and have a central mode of action. The newer, "minimally sedating" antihistamines (e.g., cetirizine, fexofenadine, loratadine) are not effective for treatment of motion sickness because they are designed to avoid penetration into the brain. Amphetamine or the highly effective combinations of amphetamine plus scopolamine (or promethazine) are not available due to legal and drug abuse reasons. Other antiemetics such as the highly potent 5-HT3 antagonists (ondansetron and granisetron) are not effective against motion sickness because their sites of action are not at the central vestibular centers of the brain. Cannabis and constituents such as delta-9-tetrahydrocannabinol, but not cannabidiol (otherwise known as CBD), have been shown to possess anti-motion-sickness properties in animals. However, controlled trials of motion sickness and cannabis in humans are currently lacking, so no firm recommendations can be made. Commonly used anti-motion-sickness drugs are shown in Table 7.6.2.
All medications used to treat motion sickness have side effects and may have specific medical contraindications. The most common side effect is drowsiness or sedation. Scopolamine is slightly less sedating than dimenhydrinate or meclizine, whereas promethazine is the most sedating. Other common side effects of anti-motion-sickness medications are dry mouth and dry eyes, but these are more common with scopolamine. Scopolamine should not be used in travelers with glaucoma or who are at risk of prostatic urinary retention. Because side effects differ among travelers, consider recommending a trial dose of 1 or more medications before departure. The transdermal patch should never be cut up in mistaken attempts to vary the dose, since this disrupts the mechanism of release.
Tablet (oral) medications should be taken in sufficient time to allow absorption. Once the initial symptoms of motion sickness begin, gastric stasis may prevent absorption. See Table 7.6.2 for onset times of action. Some cruise operators post anticipated sea conditions to allow for adequate preparation.
The following general recommendations can aid in choosing the preferred drugs for adults:
Short-term motion exposure (≤6 hours):
- Mild to moderate stimulus: meclizine or dimenhydrinate
- Intense stimulus: promethazine
Longer-term motion exposure (>6 hours):
- Mild stimulus: meclizine or dimenhydrinate
- Moderate to intense stimulus: scopolamine patch
Table 7.6.2: Characteristics of common anti-motion-sickness drugs in adults
| Drug | Example Trade Name | Route | Adult Dose | Time on Onset (h) | Duration of Action (h) |
|---|---|---|---|---|---|
| ScopolamineNonUS | Kwells | Oral | 0.3–0.6 mg | 1/2–1 | 4 |
| Scopolamine | IM | 0.1–0.2 mg | 1/4 | 4 | |
| Scopolamine | Transderm Scop | Transdermal | 1 mg | 6–8 | 72 |
| ScopolamineNonUS | Transderm V | Transdermal | 1.5 mg | 12 | 72 |
| Promethazine | Phenergan | Oral | 25–50 mg | 2 | 15 |
| Promethazine | IM | 25 mg | 1/4 | 15 | |
| Promethazine | Suppository | 25 mg | 1 | 15 | |
| DimenhydrinateOTC | Dramamine (original) | Oral | 50–100 mg | 2 | 8 |
| Dimenhydrinate | Injection | 50 mg | 1/4 | 8 | |
| Cyclizine | Marezine | Oral | 50 mg | 2 | 6 |
| Cyclizine | Injection | 50 mg | 1/4 | 6 | |
| Meclizine | Antivert | Oral | 25–50 mg | 2 | 8 |
| MeclizineOTC | Bonine, Dramamine (less drowsy) | Chewable tablet | 25–50 mg | 2 | 8–24 |
| Buclizine | Oral | 50 mg | 1 | 6 | |
| CinnarizineNonUS | Stugeron | Oral | 15–30 mg | 4 | 8 |
Notes
Abbreviations: NonUS, not available in U.S.; H, hours.
Multiple trade names may exist for the same drug, and trade names may differ between countries: dimenhydrinate (Gravol, Driminate, Dramamine original); meclizine (Bonamine, Bonine, Antivert, Postafen, Sea Legs, Dramamine Less Drowsy); cyclizine (Marezine, Cyclivert); buclizine is sometimes confusingly named Buclizine (Antivert).
Some drug formulations may be over the counter (OTC) in some countries but prescription-only in other countries.
Table modified from Benson, A. J. (2002). Medical aspects of harsh environments, motion sickness (pp. 1048–1083). Office of The Surgeon General Department of the Army, United States of America.
Children and motion sickness
Behavioral countermeasures, such as the ones mentioned before, should be tried first. Anti-motion-sickness medication for children should be used with caution. For children aged 6–12 years, dimenhydrinate (Dramamine for Kids; chewable), 12–25 mg per dose, or diphenhydramine (Benadryl), 0.5–1 mg/kg per dose up to 25 mg, can be given 1–2 hours before travel. Some expert healthcare professionals in the United States advise against the use of diphenhydramine in children since it is very sedating but can also cause paradoxical agitation; furthermore, it is not approved for children in many countries. Because some children have paradoxical agitation with antihistamines, parents are encouraged to try a test dose before departure. Over-sedating young children with antihistamines can be life-threatening. Scopolamine, including patches, can cause dangerous adverse effects such as hallucinations and mental confusion in children and should be avoided.
Mal de debarquement
Mal de debarquement (French for "sickness of disembarkation") is the persistence of imbalance or a rocking sensation after exposure to passive motion, especially after sea voyage. A transient sensation of this kind is normal, rarely involves nausea, and resolves in a few hours or less. Transient imbalance might be a risk factor to consider for elderly individuals when disembarking cruise ships. A very rare condition termed mal de debarquement syndrome involves symptoms persisting for weeks or more. For such cases, the traveler should be referred to a medical specialist in vestibular disorders.
Medical management of motion sickness
For healthcare professionals managing a traveler with acute symptoms consistent with motion sickness, other causes should be excluded, including peripheral and central vestibular disease. Travelers with a history of migraine headaches, which may provoke or exacerbate motion sickness, may benefit from migraine headache treatments, either prophylactically or after symptom onset.
Supportive measures include reassurance and having the patient lie down. Ensure adequate fluid and electrolyte intake if the individual is vomiting. In acute motion sickness, non-oral routes of administration of anti-motion-sickness drugs may be necessary because absorption of oral medications may be impaired due to gastric stasis, even in the absence of vomiting. In severe acute motion sickness, intramuscular injection should be considered (Table 7.6.2). Transdermal suppository routes of delivery are suboptimal due to slower absorption rates. Behavioral techniques may also be helpful (Table 7.6.1).
- Benson, A. J. (2002). Medical aspects of harsh environments, motion sickness (pp. 1048–1083). Office of The Surgeon General Department of the Army, United States of America.
- Cha, Y. H., Golding, J. F., Keshavarz, B., Furman, J., Kim, J. S., Lopez-Escamez, J. A., . . . Advisors. (2021). Motion sickness diagnostic criteria: Consensus document of the Classification Committee of the Bárány Society. Journal of Vestibular Research: Equilibrium & Orientation, 31(5), 327–344. https://journals.sagepub.com/doi/full/10.3233/VES-200005?rfr_dat=cr_pub++0pubmed&url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org.
- Golding J. F. (2016). Motion sickness. Handbook of Clinical Neurology, 137, 371–390. https://www.doi.org/10.1016/B978-0-444-63437-5.00027-3.
- Koch, A., Cascorbi, I., Westhofen, M., Dafotakis, M., Klapa, S., & Kuhtz-Buschbeck, J. P. (2018). The neurophysiology and treatment of motion sickness. Deutsches Arzteblatt International, 115(41), 687–696. https://www.doi.org/10.3238/arztebl.2018.0687.
- Leung, A. K., & Hon, K. L. (2019). Motion sickness: An overview. Drugs in Context, 8, 2019-9-4. https://www.doi.org/10.7573/dic.2019-9-4.
- Murdin, L., Golding, J., & Bronstein, A. (2011). Managing motion sickness. BMJ (Clinical Research Ed.), 343, 1–7. https://www.doi.org/10.1136/bmj.d7430.
- Schmäl F. (2013). Neuronal mechanisms and the treatment of motion sickness. Pharmacology, 91(3–4), 229–241. https://www.doi.org/10.1159/000350185.
- Zhang, L. L., Wang, J. Q., Qi, R. R., Pan, L. L., Li, M., & Cai, Y. L. (2016). Motion sickness: Current knowledge and recent advance. CNS Neuroscience & Therapeutics, 22(1), 15–24. https://www.doi.org/10.1111/cns.12468.