Motion sickness is a normal physiologic response to a provocative stimulus. Individual susceptibility to motion sickness varies greatly; however, it occurs more frequently in women and in children between the ages of 2 and 12 years. Motion sickness is uncommon after the age of 50 and in infants < 2 years. The incidence ranges from < 1% on airplanes to nearly 100% on ships in rough seas and upon becoming weightless during space travel.
Excessive stimulation of the vestibular apparatus by motion is the primary cause. 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 brain stem 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.
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)
Hormonal factors (eg, pregnancy, use of hormonal contraceptives)
Genetic factors may also increase susceptibility to motion sickness (1).
In space adaptation syndrome (motion sickness during space travel), weightlessness (zero gravity) is an etiologic factor. This syndrome reduces the efficiency of astronauts during the first few days of space flight, but adaptation occurs over several days.
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.
Characteristic manifestations 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.
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 another diagnosis (eg, central nervous system (CNS) hemorrhage or cerebral infarction) should be considered in some people, particularly the elderly, patients with no prior history of motion sickness, or those with risk factors for CNS hemorrhage or infarction who develop acute dizziness and vomiting during travel. Patients with focal neurologic symptoms or signs, significant headache, or other findings atypical of motion sickness should be further evaluated.
People prone to motion sickness should take prophylactic drugs and use other preventive measures before symptoms start; interventions are less effective after symptoms develop. 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, an anticholinergic prescription drug, is effective for prevention, but efficacy in treatment is uncertain. Scopolamine is available as a 1.5-mg 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 as 0.4 mg to 0.8 mg 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 the elderly can include confusion, hallucinations, and urinary retention. Scopolamine is contraindicated in people who are at risk of angle-closure glaucoma.
Scopolamine can be used by children > 12 years in the same dosages as for adults. Use in children ≤ 12 years may be safe but is not recommended due to the higher risk of adverse effects.
The mechanism of action for antihistamines is probably anticholinergic. All effective ones are sedating; nonsedating antihistamines do not appear to be effective. These drugs can be effective for prevention and possibly treatment. Anticholinergic adverse effects may be troublesome, particularly in the elderly. Beginning 1 hour before departure, susceptible people may be given nonprescription dimenhydrinate, diphenhydramine, meclizine, or cyclizine in the following doses:
Dimenhydrinate: Adults and children > 12 years, 50 to 100 mg orally every 4 to 6 hours (not to exceed 400 mg/day); children 6 to 12 years, 25 to 50 mg orally every 6 to 8 hours (not to exceed 150 mg/day); children 2 to 5 years, 12.5 to 25 mg orally every 6 to 8 hours (not to exceed 75 mg/day)
Diphenhydramine: Adults, 25 to 50 mg orally every 4 to 8 hours; children ≥ 12 years, 25 to 50 mg orally every 4 to 6 hours; children 6 to 11 years 12.5 to 25 mg orally every 4 to 6 hours; children 2 to 5 years, 6.25 mg orally every 4 to 6 hours
Meclizine: Adults and children ≥ 12 years, 25 to 50 mg orally every 24 hours
Cyclizine: Adults, 50 mg orally every 4 to 6 hours; children 6 to 12 years, 25 mg 3 or 4 times a day
Cyclizine and dimenhydrinate can minimize vagally mediated gastrointestinal symptoms.
Promethazine 25 to 50 mg orally 1 hour before departure and then twice a day appears to be effective for prevention and treatment. The dosage in children 2 to 12 years is 0.5 mg/kg orally 1 hour before departure and then twice a day; it should not be used in children < 2 years because of the risk of respiratory depression. Adding caffeine may increase efficacy. Metoclopramide may also be effective, but evidence suggests it is less so than promethazine. Adverse effects include extrapyramidal symptoms and sedation.
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.
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).
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 0.5 to 1 g, which can be repeated but should be limited to 4 g/day, has been used but has not been shown to be more effective than placebo.
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.
Drug therapy is more effective prophylactically and usually involves scopolamine or an antihistamine.
Once vomiting is established, 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.