Motion sickness is a symptom complex that usually includes nausea, often accompanied by vague abdominal discomfort, vomiting, dizziness, pallor, diaphoresis, and related symptoms. It is induced by specific forms of motion, particularly repetitive angular and linear acceleration and deceleration, or as a result of conflicting vestibular, visual, and proprioceptive inputs. Behavioral change and medications can help prevent or control symptoms.
Motion sickness is a normal physiologic response to a provocative stimulus. Depending on the setting and stimulus, it may occur in few people (eg, airplane travel without turbulence) or in nearly all people (eg, on a ship in rough seas or upon becoming weightless during space travel) (1).
Motion sickness can be stimulated by physical movement (eg riding in a car or on a boat) or if an individual has the perception of movement while stationary, also called vection.
Individual susceptibility to motion sickness varies greatly. It does, however, occur more frequently in women than men. It is more common in children between the ages of 2 and 12 years than adults; it is rare in infants < 2 years.
Symptoms of motion sickness sometimes diminish as patients get older, and new-onset motion sickness based on physical movement is uncommon after the age of 50. Older adults may be more susceptible to visually induced motion sickness (VIMS) (see Etiology).
Reference
1. Keshavarz B, Golding JF. Motion sickness: current concepts and management. Curr Opin Neurol. 2022;35(1):107-112. doi:10.1097/WCO.0000000000001018
Etiology of Motion Sickness
Excessive stimulation of the vestibular apparatus by motion is the primary cause. This stimulation may be due to actual physical motion or perceived motion. A common situation in which there is perceived motion is found in video games and virtual reality. Motion sickness that occurs in these situations are called visually induced motion sickness (VIMS) and virtual reality-induced symptoms and effects (VRISE).
Vestibular stimulation can result from angular motion (sensed by the semicircular canals) or linear acceleration or gravity (sensed by the otolithic organs [utricle and saccule]). Central nervous system (CNS) components that mediate motion sickness include the vestibular system and brainstem nuclei, the hypothalamus, the nodulus and uvula of the cerebellum, and emetic pathways (eg, medullary chemoreceptor trigger zone, vomiting center, and emetic efferents).
The exact pathophysiology is undefined, but motion sickness occurs only when the 8th cranial nerve and cerebellar vestibular tracts are intact; those lacking a functional vestibulo-cochlear system are immune to motion sickness. Movement via any form of transportation, including ship, motor vehicle, train, plane, spacecraft, and playground or amusement park rides can cause excessive vestibular stimulation.
The trigger may involve conflicting vestibular, visual, and proprioceptive inputs. For example, visual input that indicates being stationary may conflict with the sensation of movement (eg, looking at an apparently unmoving ship cabin wall while sensing the ship rolling). Alternatively, moving visual input may conflict with lack of perception of movement, eg, viewing a rapidly moving slide with a microscope or watching a virtual reality game while sitting still (also termed pseudomotion sickness or pseudokinetosis, given the lack of actual acceleration). When watching waves from a boat, a person may experience conflicting visual input (the movement of the waves in one direction) and vestibular input (the vertical motion of the boat itself).
Another possible trigger is a conflict in inputs between angular motion and linear acceleration or gravity, as can occur in a zero-gravity environment when turning (angular acceleration). Also, a pattern of motion that differs from the expected pattern (eg, in a zero-gravity environment, floating instead of falling) can be a trigger.
In space adaptation syndrome (motion sickness during space travel), weightlessness (zero gravity) is an etiologic factor. This syndrome reduces the work efficiency of astronauts during the first few days of space flight, but adaptation occurs over several days.
Risk factors
Factors that may increase the risk of developing motion sickness or increase the severity of symptoms include the following:
Poor ventilation (eg, with exposure to fumes, smoke, or carbon monoxide)
Emotional factors (eg, fear, anxiety about travel or the possibility of developing motion sickness)
Vestibulopathy (such as labyrinthitis)
Hormonal factors (eg, from pregnancy or use of hormonal contraceptives)
Genetic factors may also increase susceptibility to motion sickness (1).
There maybe an association between motion sickness and vestibular migraine (2).
References
1. Hromatka BS, Tung JY, Kiefer AK, et al. Genetic variants associated with motion sickness point to roles for inner ear development, neurological processes and glucose homeostasis. Hum Mol Genet. 24(9):2700-2708, 2015. doi: 10.1093/hmg/ddv028
2. Abouzari M, Cheung D, Pham T, et al. The Relationship Between Vestibular Migraine and Motion Sickness Susceptibility. Otol Neurotol. 2020;41(8):1116-1121. doi:10.1097/MAO.0000000000002705
Symptoms and Signs of Motion Sickness
Characteristic manifestations of motion sickness are nausea, vomiting, pallor, diaphoresis, and vague abdominal discomfort.
Other symptoms, which may precede the characteristic manifestations, include yawning, hyperventilation, salivation, and somnolence. Aerophagia, dizziness, headache, fatigue, weakness, and inability to concentrate may also occur. Pain, shortness of breath, focal weakness or neurologic deficits, and visual and speech disturbances are absent.
With continuous exposure to motion, patients often adapt within several days. However, symptoms may recur if motion increases or if motion resumes after a short respite from the inciting trigger.
Prolonged vomiting due to motion sickness may rarely lead to dehydration with hypotension, inanition, and depression.
Diagnosis of Motion Sickness
History and physical examination
The diagnosis is suspected in patients with compatible symptoms who have been exposed to typical triggers. Diagnosis is clinical and usually straightforward. However, the possibility of a more serious diagnosis (eg, central nervous system [CNS] hemorrhage or cerebral infarction) should be considered in some people, particularly older adults, patients with no prior history of motion sickness, or those with risk factors for CNS hemorrhage or infarction who develop acute dizziness (or vertigo) and vomiting during travel. Patients with focal neurologic symptoms or signs, significant headache, or other findings atypical of motion sickness should be further evaluated.
Treatment of Motion Sickness
Prophylactic medications (eg, anticholinergic, antihistamine, and antidopaminergic medications)
Nonpharmacologic prophylaxis and treatment measures
Antiemetic medications (eg, serotonin antagonists)
Sometimes IV fluid and electrolyte replacement
People prone to motion sickness should take prophylactic medications and use other preventive measures before symptoms start; interventions are less effective after symptoms develop (1). If vomiting occurs, an antiemetic, given rectally or parenterally, can be effective. If vomiting is prolonged, IV fluids and electrolytes may be required for replacement and maintenance.
Pregnant women should treat motion sickness as they would treat nausea and vomiting during early pregnancy.
Scopolamine
Scopolamine, an anticholinergic prescription medication, is effective for prevention, but efficacy in treatment is uncertain (Scopolamine, an anticholinergic prescription medication, is effective for prevention, but efficacy in treatment is uncertain (2). Scopolamine is available as a transdermal patch or in oral form. The patch is a good choice for longer trips because it is effective for up to 72 hours. It is applied behind the ear 4 hours before its effect is required. If treatment is needed after 72 hours, the patch is removed and a fresh one is placed behind the other ear. The oral form of scopolamine is effective within 30 minutes and is given 1 hour before travel and then every 8 hours as needed.). Scopolamine is available as a transdermal patch or in oral form. The patch is a good choice for longer trips because it is effective for up to 72 hours. It is applied behind the ear 4 hours before its effect is required. If treatment is needed after 72 hours, the patch is removed and a fresh one is placed behind the other ear. The oral form of scopolamine is effective within 30 minutes and is given 1 hour before travel and then every 8 hours as needed.
Anticholinergic adverse effects, which include drowsiness, blurred vision, dry mouth, and bradycardia, occur less commonly with patches. Inadvertent contamination of the eye with patch residue may cause a fixed and widely dilated pupil. Additional adverse effects of scopolamine in older adults can include confusion, hallucinations, and urinary retention. Scopolamine is contraindicated in people who are at risk of Anticholinergic adverse effects, which include drowsiness, blurred vision, dry mouth, and bradycardia, occur less commonly with patches. Inadvertent contamination of the eye with patch residue may cause a fixed and widely dilated pupil. Additional adverse effects of scopolamine in older adults can include confusion, hallucinations, and urinary retention. Scopolamine is contraindicated in people who are at risk ofangle-closure glaucoma.
Pearls & Pitfalls
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Scopolamine can be used by children Scopolamine can be used by children> 12 years in the same dosages as for adults. Use in children ≤ 12 years is not recommended due to the higher risk of adverse effects.
Antihistamines
The mechanism of action for antihistamines is probably anticholinergic. All effective ones are sedating; nonsedating antihistamines do not appear to be effective. These medications can be effective for prevention and possibly treatment. Anticholinergic adverse effects may be troublesome, particularly in older adults. Beginning 1 hour before departure, susceptible people may be given nonprescription dimenhydrinate, diphenhydramine, meclizine, or cyclizine.The mechanism of action for antihistamines is probably anticholinergic. All effective ones are sedating; nonsedating antihistamines do not appear to be effective. These medications can be effective for prevention and possibly treatment. Anticholinergic adverse effects may be troublesome, particularly in older adults. Beginning 1 hour before departure, susceptible people may be given nonprescription dimenhydrinate, diphenhydramine, meclizine, or cyclizine.
If there is excessive sedation, subsequent doses can be reduced. Cyclizine and dimenhydrinate can minimize vagally mediated gastrointestinal symptoms.If there is excessive sedation, subsequent doses can be reduced. Cyclizine and dimenhydrinate can minimize vagally mediated gastrointestinal symptoms.
Antidopaminergic medications
Promethazine orally 1 hour before departure and then twice a day appears to be effective for prevention and treatment. Weight-based dosing should be used for children 2 to 12 years; it should not be used in children < 2 years because of the risk of respiratory depression. Adding caffeine may increase efficacy (Promethazine orally 1 hour before departure and then twice a day appears to be effective for prevention and treatment. Weight-based dosing should be used for children 2 to 12 years; it should not be used in children caffeine may increase efficacy (3). Metoclopramide may also be effective, but may be less effective than promethazine. Adverse effects include extrapyramidal symptoms and sedation.). Metoclopramide may also be effective, but may be less effective than promethazine. Adverse effects include extrapyramidal symptoms and sedation.
Benzodiazepines
Benzodiazepines (eg, diazepam) may also have some benefit in the treatment of motion sickness but do have sedative effects.Benzodiazepines (eg, diazepam) may also have some benefit in the treatment of motion sickness but do have sedative effects.
Serotonin antagonists
Serotonin (5-HT3) antagonists, such as ondansetron and granisetron, are highly effective antiemetics, but the few studies addressing their use in preventing motion sickness have not shown significant efficacy. However, in cases of severe nausea and vomiting, using serotonin antagonists is reasonable.Serotonin (5-HT3) antagonists, such as ondansetron and granisetron, are highly effective antiemetics, but the few studies addressing their use in preventing motion sickness have not shown significant efficacy. However, in cases of severe nausea and vomiting, using serotonin antagonists is reasonable.
Nonpharmacologic measures
Susceptible people should minimize exposure by positioning themselves where motion is the least (eg, in the middle of a ship close to water level, over the wings in an airplane). Also, they should try to minimize the discrepancy between visual and vestibular stimuli. If traveling in a motor vehicle, then driving or riding in the front passenger seat, where vehicle motion is most evident (or where motion is most visible), is best. When traveling on a ship, viewing the horizon or land masses is usually better than viewing a cabin wall. Whatever the form of transportation, reading and rear-facing seats should be avoided. A supine or semirecumbent position with the head supported is best. Sleeping can also help by reducing vestibular sensory input. In space adaptation syndrome, movement, which aggravates the symptoms, should be avoided.
Adequate ventilation helps prevent symptoms. Consuming alcoholic beverages and overeating before or during travel increase the likelihood of motion sickness. Small amounts of fluids and bland food consumed frequently are preferred to large meals during extended travel; some people find that dry crackers and carbonated beverages, especially ginger ale, are best. If travel time is short, food and fluids should be avoided.Adequate ventilation helps prevent symptoms. Consuming alcoholic beverages and overeating before or during travel increase the likelihood of motion sickness. Small amounts of fluids and bland food consumed frequently are preferred to large meals during extended travel; some people find that dry crackers and carbonated beverages, especially ginger ale, are best. If travel time is short, food and fluids should be avoided.
Adaptation is one of the most effective prophylactic therapies for motion sickness and is accomplished by repeated exposure to the same stimulus. However, adaptation is specific to the stimulus (eg, sailors who adapt to motion on large boats may still develop motion sickness when on smaller boats).
Alternative therapies
Some alternative therapies are unproven but may be helpful. These alternative therapies include wristbands that apply acupressure and wristbands that apply electrical stimulation. Both can be safely used by people of all ages. Ginger has been used but there are limited high-quality studies (Some alternative therapies are unproven but may be helpful. These alternative therapies include wristbands that apply acupressure and wristbands that apply electrical stimulation. Both can be safely used by people of all ages. Ginger has been used but there are limited high-quality studies (4).
Treatment references
1. Leung AK, Hon KL. Motion sickness: an overview. Drugs Context. 2019;8:2019-9-4. Published 2019 Dec 13. doi:10.7573/dic.2019-9-4
2. Spinks A, Wasiak J. Scopolamine (hyoscine) for preventing and treating motion sickness. . Scopolamine (hyoscine) for preventing and treating motion sickness.Cochrane Database Syst Rev. 2011;2011(6):CD002851. Published 2011 Jun 15. doi:10.1002/14651858.CD002851.pub4
3. Estrada A, LeDuc PA, Curry IP, et al. Airsickness prevention in helicopter passengers. Aviat Space Environ Med. 2007;78(4):408-413.
4. Lien HC, Sun WM, Chen YH, et al. Effects of ginger on motion sickness and gastric slow-wave dysrhythmias induced by circular vection. Am J . Effects of ginger on motion sickness and gastric slow-wave dysrhythmias induced by circular vection. Am JPhysiol Gastrointest Liver Physiol. 2003;284(3):G481-G489. doi:10.1152/ajpgi.00164.2002
Key Points
Motion sickness is triggered by excessive stimulation of the vestibular system or conflicts among proprioceptive, visual, and vestibular sensory inputs.
The diagnosis, based on clinical findings, is usually straightforward.
Medication therapy is more effective prophylactically and usually involves scopolamine or an antihistamine.Medication therapy is more effective prophylactically and usually involves scopolamine or an antihistamine.
Once vomiting has started, serotonin antagonist antiemetics are preferred.
To minimize motion sickness, it is recommended that people seek the position in the vehicle least subject to motion, sleep when possible, obtain adequate ventilation, and avoid alcohol and unnecessary food and drink.
