Motion sickness

Douglas J Lanska MD FAAN MS MSPH (

Dr. Lanska of the University of Wisconsin School of Medicine and Public Health, the Medical College of Wisconsin, and IM Sechenov First Moscow State Medical University has no relevant financial relationships to disclose.

Originally released September 10, 2009; last updated October 21, 2020; expires October 21, 2023


In this article, the author explains the clinical presentation, pathophysiology, and management of motion sickness. Motion sickness is a normal response to complex motion stimuli of sufficient intensity and duration that is thought to be due to a mismatch of signals from vestibular, visual, and proprioceptive receptors as integrated in the brainstem and cerebellum.

Key points


• Motion sickness is a normal response to complex motion stimuli of sufficient intensity and duration.


• Motion sickness typically occurs with unfamiliar motion to which an individual has not adapted.


• Motion sickness can produce uncomfortable or unpleasant and sometimes incapacitating manifestations, but the most common include pallor, cold sweating (diaphoresis), anorexia, nausea, and vomiting.


• The earliest symptom is typically epigastric discomfort (“stomach awareness”), followed by malaise and a feeling of warmth, often coincident with the onset of nausea. The development of pallor, diaphoresis, and changes in respiratory rhythm herald the onset of vomiting, which generally produces some temporary symptomatic improvement.


• In some cases that do not reach the threshold of vomiting, manifestations may be limited to fatigue and drowsiness, ie, the “sopite syndrome.”


• Susceptibility to motion sickness varies with age (with peak prevalence between ages 4 and 12 years), gender (women more often affected, especially during menstruation, in most studies). Other risk factors include a history of motion sickness, a history of migraine headaches, family history of motion sickness, and Asian heritage.


• Motion sickness is thought to be due to a mismatch of signals from vestibular, visual, and proprioceptive receptors as integrated in the brainstem and cerebellum.


• Motion sickness is distinct from mal de debarquement because subjects with motion sickness experience symptoms during the period of motion and briefly afterwards, whereas mal de debarquement subjects experience symptoms following termination of motion. Furthermore, subjects with mal de debarquement do not commonly have associated nausea, vomiting, diaphoresis, or headache, all of which are common with motion sickness.


• To minimize visual-vestibular mismatch, it helps to be able to have correct visual cues for orientation; therefore, it helps to direct attention to a stable orientational reference (eg, looking at the horizon while aboard ship or looking out through the windshield at a distant point ahead while a passenger in the front seat of a car as opposed to looking out a side window from the back seat or, worse, trying to read), to avoid enclosed cabins, and to avoid focusing on nearby objects (eg, waves, other vehicles) and, especially, tasks involving visual search of nearby objects (eg, reading or map reading).


• Transdermal scopolamine (l-hyoscine) is probably the most effective available medication for prevention of motion sickness.

Historical note and terminology

Motion sickness, or kinetosis, is a normal response to complex motion stimuli of sufficient intensity and duration. It typically occurs with unfamiliar motion to which an individual has not adapted. Motion sickness can produce uncomfortable or unpleasant and sometimes incapacitating manifestations, but the most common include pallor, cold sweating (diaphoresis), anorexia, nausea, and vomiting. There is a wide range of susceptibility to motion sickness and also considerable variability in the relative prominence of the clinical manifestations, but all healthy unmedicated individuals can become motion sick with sufficient provocative stimuli (Murdin et al 2011).

Motion sickness may have evolved as a negative reinforcement system designed to terminate motion involving sensory conflict or postural instability that would have impaired evolutionary fitness via injury or signaling weakness and vulnerability to predators (Bowins 2010; Murdin et al 2011). Such a negative reinforcement mechanism would have functioned much like pain to strongly motivate behavior-preserving evolutionary fitness. Alternate theories positing that motion sickness facilitated the avoidance or elimination of neurotoxins cannot account for the rarity of motion sickness in infants and toddlers.

Motion sickness has been recognized for centuries, especially in the form of seasickness (Huppert et al 2017). Indeed, the etymology of the English word nausea is from the Greek word naus, meaning ship, or nautēs, meaning sailor. As expressed by Hill:


Ever since the first Palaeolithic man ventured afloat in a hollow tree-trunk, Homo sapiens has been striving to adapt his reflexes to movement in three planes. But his sapient mind travels with more ease and comfort in four dimensions than his human body does in three. …It is as natural for the novice to be sea-sick in stormy weather as for the toddler to stumble or the inexpert golfer to foozle his drive (Hill 1936).

Chinese medical classics recognized the particular susceptibility of children to motion sickness and distinguished several forms of travel sickness (Brandt et al 2016; Huppert et al 2017). By 300 A.D., the Chinese recognized cart sickness, experienced by persons traveling in arid northern China, as distinct from sea sickness, experienced by persons traveling by boat in southern China, where rivers were important for transportation. In the Middle Ages, a third form of motion sickness was recognized: litter sickness, experienced by persons transported in a bed suspended between 2 long poles.

On November 16, 1809, in his Croonian Lecture to the Royal Society, English chemist and physicist William Hyde Wollaston (1766–1828) attributed motion sickness to motion-induced fluctuations in the pressure within cerebral blood vessels (Wollaston 1810; Lanska 2014a):

English chemist and physicist William Hyde Wollaston Image: English chemist and physicist William Hyde Wollaston (1766–1828)


If a person be supposed standing erect upon deck [of a ship], it is evident that the brain, which is uppermost, then sustains no pressure from the mere weight of the blood, and that the vessels of the feet and lower parts of the body must contract, with a force sufficient to resist the pressure of a column of blood, of between five and six feet from the head downwards. If the deck were by any means, suddenly and entirely removed, the blood would be no longer supported by its vessels; but both would wall together with the same velocity by the free action of gravity; and the same contraction of the vessels which before supported the weight of the blood would now occasion it to press upon the brain, with a force proportional to its former altitude. In the same manner, and for the same reason, during a more gradual subsidence of the deck, and partial removal of support, there must be a partial diminution of the pressure of the blood upon its vessels, and consequently, a partial reaction upon the brain, which would be directly counteracted by a full inspiration. … The sickness occasioned by swinging is evidently from the same causes as sea-sickness, and that direction of the motion which occasions the most piercing sensation of uneasiness, is conformable to the explanation above given (Wollaston 1810).

In 1881, Irish-American physician John Arthur Irwin (1853–1912) suggested that sensory conflict was the principle etiologic factor in the development of seasickness, or more generally in what he labeled “motion sickness” (Irwin 1881; Anonymous 1892; Lanska 2014b).

Irish-American physician John Arthur Irwin Image: Irish-American physician John Arthur Irwin (1853–1912)
Irwin recognized that the “'faculty of equilibrium' appears to be more of less connected with the cerebellum, the optic lobes, and possibly with other parts of the nervous organization, but beyond doubt its principal seat is in the semicircular canals of the internal ear, which may for practical purposes be regarded as ‘the organs of equilibrium.'”

In 1882, American philosopher and psychologist William James (1842–1910) supported this concept when he reported that deaf-mutes were resistant to the development of seasickness, providing further evidence that the vestibular apparatus was somehow involved in the pathophysiology of this condition (James 1882; Lanska 2014b).

American philosopher and psychologist William James Image: William James (1842-1910)

Many other means of conveyance besides boats and ships, and later other motion stimuli (eg, visual optokinetic stimuli and 3-D movies) (Cheung et al 1991; Reid et al 1995; Hu et al 1996; Hu et al 1999; Muth et al 1996; Park and Hu 1999; Bubka and Bonato 2003; Bos and Bles 2004; Brooks et al 2010; Golding 2012; Solimini 2013; Brandt et al 2016; Bronstein et al 2020), were linked with the development of motion sickness, and in many cases each was given its own name. Such subcategories of motion sickness include, for example, cart sickness, litter sickness, airsickness, car sickness, camel sickness, cyber sickness (virtual reality), elevator sickness, simulator sickness, ski sickness, space sickness, swing sickness, train sickness, and motorist's disorientation syndrome (Reason 1978; Haüsler 1995; Benson 2002; Brooks et al 2010; Chen et al 2016; Bertolini et al 2017; Reschke et al 2018; Russomano et al 2019; Bronstein et al 2020). Sickness affects about one third of zero-G fliers (Golding et al 2017), and 50% to 70% of all space travelers during the first 24 to 72 hours of a spaceflight (Thornton and Bonato 2013; Russomano et al 2019).

Despite centuries of interest in the condition, prevention and management of motion sickness have been and remain less than ideal (Golding and Gresty 2015). In a news item in the 1881 Pacific Medical and Surgical Journal the treatment of seasickness by different prominent neurologists of the time was summarized, based on a report in the New York Medical Record and additional commentary:


Several physicians have been interviewed by newspaper reports on the subject of seasickness. Dr. Alonzo Clark recommends a wash-bowl, Dr. [George Miller] Beard bromization, and Dr. [William Alexander] Hammond chloroform and bromides. The editors comment upon the uncertainties of medicine and the disagreement of doctors. Without entirely disregarding bromides, we think highly of the washbowl… When the senior editor shipped at New York for California thirty-one years ago, he observed in his state-room a tin vessel with hooks for handles, the use of which at first was a great puzzle; but in the course of time he found it much more convenient than a wash-bowl (Anonymous 1881).

Belladonna alkaloids were also found empirically to be beneficial, but as cautioned by Hill: “there is no panacea to be found in ‘all the drowsy syrups of the world,' or even all the alkaloids of belladonna” (Hill 1936).

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