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Motion sickness

Motion sickness
Literature review current through: Jan 2024.
This topic last updated: Jun 23, 2023.

INTRODUCTION — Motion sickness is a syndrome that occurs in response to real or perceived motion, which can include gastrointestinal, central nervous system, and autonomic symptoms.

Motion sickness is considered a physiologic form of dizziness, since it is not indicative of a disease process and can be induced in nearly all normal human subjects. There is enormous variability in susceptibility to motion sickness, as it may be produced with minimal provocation in some individuals but can be very difficult to elicit in others.

The symptoms of motion sickness were first described by Hippocrates. They frequently occur during boat travel, and the principal symptom (nausea) is derived from the Greek word for ship (naus).

This topic discusses the pathogenesis, epidemiology, clinical presentation, diagnosis, prevention, and treatment of motion sickness. A possibly related disorder, disembarkment syndrome (sometimes called mal de debarquement syndrome), and other causes of vertigo and dizziness are discussed separately. (See "Causes of vertigo".)

PATHOGENESIS — The brain receives numerous inputs that are used to estimate the motion and spatial orientation of the head. The principal sensory signals that contribute to this process are vestibular cues from the labyrinth, visual information, and somatosensory cues. Afferent information derived from the labyrinth encodes both angular motion (sensed by the semicircular canals) and linear acceleration and gravitational force (sensed by the otolith organs).

During active movements such as locomotion, the motor command generated by the brain (sometimes referred to as a corollary discharge or efference copy) is also used to estimate the motion of the head and body. During self-generated movements in normal subjects, the motor command and sensory feedback are congruent, and the brain can generate a stable and accurate estimate of head motion and orientation.

In the absence of active movements, the brain's estimate of motion is primarily based upon vestibular, visual, and somatosensory information. When these three sensory cues are not congruent, a sensory conflict is generated in the brain, and it is hypothesized that this conflict underlies the symptoms of motion sickness [1-3].

As an example, if the visual system indicates that a person is stationary (eg, viewing the interior of a cabin on a ship), but the vestibular system senses ongoing head movements (eg, due to motion of the ship), the vestibular and visual cues conflict and engender symptoms of motion sickness. Furthermore, if the semicircular canals and otolith organs produce sensory cues that are incongruous, motion sickness can be evoked that is independent of vision.

Similarly, if the visual system indicates movement (eg, moving a microscope slide, engaging in virtual reality games or rides, watching a point-of-view movie) but the vestibular system does not, a visually induced motion sickness can result.

Labyrinthine inputs are clearly crucial to the development of motion sickness, since experimental animals with inactivated semicircular canals or otolith organs do not develop the syndrome [4,5], nor did a group of deaf subjects who were presumed to lack peripheral vestibular function [6]. Conversely, blind subjects have a predilection to motion sickness similar to those with normal vision, suggesting that the contribution of visual information to this syndrome is less critical [7]. Movements that are most likely to elicit motion sickness include low-frequency rotations and translations and novel motion patterns, particularly those involving head rotations about two axes simultaneously (resulting in cross-coupled, or Coriolis, forces) [8].

The anatomic basis for motion sickness is not well understood. It is presumed to depend upon connections between the central vestibular system in the brainstem and cerebellum and the autonomic and emetic centers in the brain [9]. Projections from the nodulus and uvula of the cerebellum to the brainstem that modulate a central vestibular process referred to as "velocity storage" may be critical for the development of motion sickness [10,11]. Histamine, acetylcholine, and norepinephrine appear to be the critical neurotransmitters involved in the production of motion sickness [12]. Gamma-aminobutyric acid (GABA) also plays a role in motion sickness through effects on the velocity storage integrator [13].

EPIDEMIOLOGY — Motion sickness can be induced in almost all people with sufficient provocation. Individuals vary in their susceptibility to motion sickness, and certain characteristics are correlated with this susceptibility.

Incidence — The incidence of motion sickness depends upon the specific conditions encountered. The following observations illustrate the findings in different settings:

In a study of 20,029 passengers on 114 voyages at sea (six ships, two hovercraft, and one jet foil), 21 percent felt "slightly unwell," 4 percent felt "quite ill," 4 percent felt "absolutely dreadful," and 7 percent experienced vomiting [14].

In a study of 3256 passengers on 56 bus trips, 28 percent reported feeling ill, 13 percent reported nausea, and 2 percent reported vomiting [15].

In a study of 923 passengers on 38 commercial airline flights, 16 percent reported feeling ill, 8 percent reported nausea, and 0.5 percent reported vomiting [16].

Risk factors

Patient factors

Sex – Females are generally more susceptible to motion sickness than males [17].

Age – Children less than two years old are typically resistant to motion sickness; the incidence peaks at approximately nine years of age and then decreases throughout adulthood [18].

Genetic factors – Genetic variants have been associated with increased susceptibility to motion sickness; a genome-wide study of 80,494 individuals found 35 single-nucleotide polymorphisms (SNPs) that were associated with motion sickness [19].

Migraine – Migraine sufferers are more susceptible to motion sickness [20-23]. In one study, 50 percent of migraine sufferers reported a history of motion sickness versus 20 percent of persons with tension headache [24].

Hormonal factors – Individuals are particularly susceptible to motion sickness during pregnancy; susceptibility may also be affected by the menstrual cycle and by use of oral contraceptives [25,26].

Expectations – The risk of motion sickness may be affected by an individual’s expectations of whether or not they will become ill. As an example, a controlled trial found that naval cadets who were told they were unlikely to experience seasickness were at decreased risk of developing motion sickness [27].

Environmental factors

Type of motion – As discussed above, low-frequency motion and certain directions of motion are more likely to induce motion sickness. In a study of air travelers, the magnitude of low-frequency lateral and vertical motion was associated with motion sickness [16].

Body position – Lying supine, at least on a ship, may decrease susceptibility to motion sickness [28].

CLINICAL PRESENTATION — The syndrome of motion sickness is easily recognized, since it includes stereotypic symptoms in the setting of passive motion or in the setting of visual perception of motion without actual movement.

The most characteristic symptom of motion sickness is nausea. This can begin subtly; it is often described as a sense of being aware of one’s stomach. Other common features include a feeling of warmth and malaise [16]. Nausea can progress to vomiting, which is occasionally severe. Some patients may experience headache with their motion sickness.

Other symptoms may include nonvertiginous dizziness, belching, increased salivation, diaphoresis, and a general feeling of malaise [25,29]. Hyperventilation is a common associated feature and can induce dyspnea, paresthesias, and feelings of impending doom.

Physical signs usually cannot be detected, although pallor may be present. Subtle autonomic changes can be quantified with appropriate testing and include increased perspiration, slowing of gastric emptying, and postural hypotension [30,31].

Symptoms typically subside after 36 to 72 hours of continuous exposure, but they can recur upon returning to the pre-exposure environment (eg, returning to land after a sea voyage) [25].

DIAGNOSIS — The diagnosis of motion sickness is clinical, based upon the presence of typical symptoms (eg, nausea, sweating, malaise) in response to externally imposed motion or other stimulus. If a patient has a previous history of motion sickness and a typical presentation, then no further evaluation is needed.

However, if a patient with no prior motion sickness suddenly becomes prone to motion sickness, then evaluation for migraine, which is associated with increased susceptibility to motion sickness, is warranted. There is evidence that better control of migraine can reduce motion sickness susceptibility [32,33].

DIFFERENTIAL DIAGNOSIS — True vertigo is a distinguishing characteristic of other disorders, such as vestibular migraine and vestibulopathy, that may be confused with motion sickness. However, true vertigo is not a feature of motion sickness.

Vestibular migraine shares some clinical features with motion sickness, but patients with vestibular migraine usually have a migraine-type headache and true vertigo rather than nonvertiginous dizziness. (See "Vestibular migraine", section on 'Clinical features'.)

Vestibulopathy can increase visual-vestibular conflict and should be considered in patients who report motion sickness but who have not been prone to it in the past. Vestibulopathy may be a benign, self-limited disorder (vestibular neuritis) or may result from exposure to ototoxic medications. If vestibulopathy is suspected, referral to a neurologist or vestibular specialist is indicated. Patients with vestibulopathies typically experience symptoms with all types of motion, not solely with externally imposed or perceived motion, as in motion sickness. (See "Causes of vertigo", section on 'Peripheral etiologies'.)

APPROACH TO MANAGEMENT — A patient may consult a clinician about prevention of motion sickness or about treatment of acute motion sickness. Treatment of acute motion sickness is often ineffective, and therefore an emphasis should be placed on prevention [34].

Prevention — Patients vary considerably in their susceptibility to motion sickness:

Significant motion sickness – Some patients report a prior history of motion sickness symptoms that are distressing and interfere with their ability to function. (See 'Patients with a history of significant motion sickness' below.)

No significant motion sickness – Other patients do not report a prior history of motion sickness or have had mild symptoms that do not interfere with their ability to function. (See 'Patients without a history of significant motion sickness' below.)

The management of the patient should take into account whether or not they have a history of significant motion sickness. All patients should be counseled about environmental modification and all patients should be offered complementary and alternative treatments. However, because all medications used to prevent motion sickness are sedating, we base the decision about using medication upon the likelihood that the patient will be affected by motion sickness. In patients without a past history of significant motion sickness, the risk of illness is low and does not justify the risk of side effects from medication.

Patients with a history of significant motion sickness — Patients who have experienced significant motion sickness in the past often ask clinicians for advice on how to prevent motion sickness. In general, interventions that are useful in preventing motion sickness can be divided into environmental modifications, complementary and alternative treatments, and medications.

Environmental modification — Patients should be advised about environmental modification measures, which include:

Looking at the horizon or a distant, stationary object.

Avoidance of reading or looking at a screen while in a moving environment, as this can increase conflict between vestibular and visual cues.

Selecting seats where motion is the least. In a boat, lower deck and midship cabins are recommended. In a car, the front seat is recommended. In a plane, a seat over the front edge of the wing is recommended. If travelling by train or bus, forward facing seats are recommended.

Driving the car is better than being the passenger, presumably because visual information is consistent with vestibular motion detection. When a passenger, it is preferable to be in the front seat with one’s eyes on the road, as if driving the car.

Data on the efficacy of environmental modifications are limited, but studies have suggested benefit from looking at a stable visual reference point, avoidance of reading while in motion, and driving rather than being a passenger [35-38]. In addition, seating locations with more motion are associated with higher risk for motion sickness [15,16].

Complementary and alternative treatments — In addition to environmental modification, we discuss the use of ginger and acupressure bands with patients prone to motion sickness, as these measures are well tolerated and may be beneficial.

Specifically, we advise patients suck on hard ginger candies if they experience or anticipate experiencing symptoms of motion sickness. Acupressure bands are typically applied to both wrists prophylactically but can also be worn after symptoms have begun.

Randomized trials both in experimental motion sickness and in naval cadets at sea have found benefit with pretreatment with 1 to 2 grams of ginger [39,40]. The mechanism of benefit with ginger is uncertain. Some studies suggest that it has an effect on gastric motility [41,42], while other studies suggest a central effect of its active constituents on serotonin receptor subtypes [43].

Acupressure for motion sickness applies pressure at the P6 acupressure point on the anterior wrist (three fingerbreadths proximal to the proximal wrist fold, between the palmaris longus and flexor carpi radialis tendons) (picture 1) either by manual pressure or with a wrist band. It has been reported to be effective for motion sickness in some [44-46], but not all [47-49], controlled trials. A randomized trial with a device that applies electrical stimulation to the P6 point found no benefit [50].

While these results raise the possibility that acupressure may be of benefit for motion sickness, trials of this sort are difficult to perform with adequate blinding and allocation concealment. It remains uncertain whether acupressure provides a benefit beyond a placebo effect [30,31].

Scopolamine or antihistamines — Medications are helpful in the prevention of motion sickness but are often sedating, so the patient’s likelihood of experiencing motion sickness must be balanced against the possibility of side effects. The best studied and most commonly used options are scopolamine and antihistamines.

The specific medication chosen will depend upon the circumstances (eg, the duration of the exposure and the acceptability of drowsiness or other side effects). As an example, the extended duration of action of the scopolamine patch may be beneficial if the exposure to motion will be prolonged, such as with an ocean voyage. Although shorter-acting and potentially more sedating, antihistamines have the advantages of lower cost, over-the-counter availability, and relatively rapid onset of action. Antihistamines are therefore frequently used when a limited exposure to motion is anticipated.

Scopolamine (transdermal) – Scopolamine is usually prescribed as a 1 mg transdermal patch, applied behind the ear at least four hours (preferably 12 hours) before exposure to motion. Patches should be replaced every 72 hours if needed. Because motion sickness may cause gastric hypomotility, the transdermal route is advantageous. For patients with symptoms that persist despite a single patch, a second patch may be added; this increased dose is generally well tolerated [51].

Transdermal scopolamine is generally well tolerated. Potential side effects of scopolamine include sedation, blurred vision, dry mouth and, in older adults, confusion and urinary retention. Some patients develop dermatitis from the scopolamine patch. Scopolamine is contraindicated in people at risk for angle-closure glaucoma.

A meta-analysis of 14 trials involving 1025 subjects found that scopolamine was more effective in preventing motion sickness than placebo (risk ratio [RR] 0.48, 95% CI 0.32 to 0.73) but not more effective than antihistamines [52].

Antihistamines – A number of antihistamines can be given to prevent motion sickness. We use dimenhydrinate or meclizine, 25 mg orally every six to eight hours as needed, with the first dose taken 30 to 60 minutes prior to anticipated travel. If sedation is excessive, the dose may be reduced to 12.5 mg or even 6.25 mg. Other antihistamines used for motion sickness include diphenhydramine, chlorpheniramine [53], cyclizine [54], and cinnarizine [55]. Dimenhydrinate is available as a chewable tablet. Cinnarizine is not available in the United States but is widely used in other countries; cyclizine is not available in the United States or Canada.

Nonsedating antihistamines (eg, cetirizine, loratadine, fexofenadine) do not appear to be effective for the treatment of motion sickness [56,57].

Side effects are mainly related to anticholinergic effects and include sedation, blurred vision, dry mouth and, in older adults, confusion and urinary retention. One small study suggested that cyclizine may be less sedating than dimenhydrinate at a dose that is equally effective for symptoms of motion sickness [58].

Antihistamines are effective for the prevention of motion sickness but may cause more sedation than scopolamine [59].

Patients who have failed transdermal scopolamine and antihistamines — Promethazine is less well studied for prevention of motion sickness but is a reasonable choice if transdermal scopolamine and antihistamines are not effective. It may be more sedating than antihistamines. In addition to sedation, side effects of promethazine include anticholinergic and extrapyramidal effects. (See "Characteristics of antiemetic drugs", section on 'Antihistamines'.)

Oral scopolamine is used infrequently but is an option if the duration of exposure to motion will be brief and antihistamines are not tolerated or are ineffective. Typical dosing is 0.25 to 0.8 mg one hour before exposure to motion and then 0.25 to 0.8 mg three times daily as needed and tolerated. Oral scopolamine has been discontinued in the United States but may be available from compounding pharmacies.

Other medications that have been shown to be effective for prevention in small trials include diazepam, phenytoin, and rizatriptan (in people who have migraines); ondansetron is not effective in the prevention of motion sickness [33,60-63].

Patients who need to avoid sedation — Preventing motion sickness can be a particular problem in patients who need to perform tasks such as flying a plane or acting as crew on a ship, since the medications used are all potentially sedating [64-66]. Dimenhydrinate, for example, may have particularly negative effects on performance [67].

In such individuals, we would use a sedating antihistamine in combination with a stimulant such as pseudoephedrine or ephedrine. This combination is available in some over-the-counter preparations (eg, chlorpheniramine and pseudoephedrine). Although amphetamine has been studied in this population, we do not use amphetamines to prevent the side effects of drugs used for motion sickness.

Limited data suggest that stimulants may counteract the side effects of sedating medicines used to prevent motion sickness. As an example, one trial found that administering amphetamine, but not pseudoephedrine, with promethazine appeared to prevent the sleepiness and impairment of psychomotor performance seen with promethazine alone [68]. Another trial reported that ephedrine decreased sleepiness and improved performance in patients administered chlorpheniramine, although it did not add to the effectiveness of chlorpheniramine in treating motion sickness [69].

Patients without a history of significant motion sickness — Although infrequently, some patients may ask about preventing motion sickness, even if motion sickness has not been a significant problem previously.

In such cases, it is reasonable to provide information about environmental modification measures and complementary and alternative treatments, which are discussed above. (See 'Environmental modification' above and 'Complementary and alternative treatments' above.)

We generally do not recommend medications to patients who are not prone to significant motion sickness because of the potential for sedation and other anticholinergic side effects.

Pregnant patients — As mentioned above, pregnant patients may be particularly susceptible to motion sickness. Medications that are felt to be safe for the treatment of morning sickness can also be used for motion sickness. These include the antihistamines meclizine and dimenhydrinate. Alternatives include scopolamine and promethazine. However, scopolamine should be avoided in patients with severe preeclampsia due to increased risk of eclamptic seizures [70]. (See "Nausea and vomiting of pregnancy: Clinical findings and evaluation".)

Treatment — In a patient with symptomatic motion sickness, the same interventions employed for prevention of significant symptoms are used: environmental modification, complementary and alternative treatments, and rapidly acting medications such as antihistamines. (See 'Patients with a history of significant motion sickness' above.)

Medications used to prevent motion sickness may be less effective in patients with acute symptoms because motion sickness induces gastric stasis, which interferes with the absorption of drugs given orally.

Promethazine can be used if antihistamines are ineffective, although the data are limited [71]. Promethazine has the advantage of availability as an intramuscular injection or as a suppository. However, there is a risk of soft tissue injury or gangrene with intramuscular administration. Dosing in all forms is 25 mg, given every 8 to 12 hours as needed.

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topic (see "Patient education: Motion sickness (The Basics)")

SUMMARY AND RECOMMENDATIONS

Definition and pathogenesis – Motion sickness is a syndrome that occurs in response to real or perceived motion, which can include gastrointestinal, central nervous system, and autonomic symptoms. In the absence of active, self-generated movements, the brain's estimate of motion is primarily based upon vestibular, visual, and somatosensory information. When these three sensory cues are not congruent, a sensory conflict is generated in the brain, and it is hypothesized that this conflict underlies the symptoms of motion sickness. (See 'Introduction' above and 'Pathogenesis' above.)

Epidemiology – Motion sickness can be induced in almost all people with sufficient provocation. Individuals vary in their susceptibility to motion sickness. In general, females (especially during pregnancy), children older than two years, and migraine sufferers are more susceptible. (See 'Epidemiology' above.)

Clinical presentation and diagnosis – Common symptoms of motion sickness include nausea, headache, warmth, and malaise. Other symptoms may include a nonvertiginous sense of dizziness, belching, increased salivation, and diaphoresis. (See 'Clinical presentation' above.)

The diagnosis of motion sickness is clinical, based upon the presence of typical symptoms in response to externally imposed motion or perceived motion. If a patient has a previous history of motion sickness and a typical presentation, then no further evaluation is needed. However, if a patient with no prior motion sickness suddenly becomes prone to motion sickness, then evaluation for migraine, which is associated with increased susceptibility to motion sickness, is warranted. (See 'Diagnosis' above.)

Management: Emphasis on prevention – Treatment of acute motion sickness is often ineffective, and therefore an emphasis should be placed on prevention. Our approach to the prevention of motion sickness depends upon the patient’s past susceptibility to motion sickness (see 'Prevention' above):

History of significant motion sickness – Some patients report a prior history of motion sickness symptoms that are distressing and interfere with their ability to function. In such patients, we employ:

-Environmental modifications (eg, looking at the horizon, avoidance of reading, and selecting a seat where motion is the least). (See 'Environmental modification' above.)

-Complementary and alternative treatments (ginger candies and acupressure bands). (See 'Complementary and alternative treatments' above.)

-Medications – The best studied and most commonly used medication options are scopolamine and antihistamines. The specific medication chosen will depend upon the circumstances (eg, the duration of the exposure and the acceptability of drowsiness or other side effects). (See 'Scopolamine or antihistamines' above.)

No history of significant motion sickness – Other patients do not report a prior history of motion sickness or have had mild symptoms that do not interfere with their ability to function. For such patients, we provide information about environmental modification measures and complementary and alternative treatments. We generally do not recommend medications to patients who are not prone to significant motion sickness because of the potential for sedation and other anticholinergic side effects. (See 'Patients without a history of significant motion sickness' above.)

Pregnancy – Pregnant individuals may be particularly susceptible to motion sickness. Medications that are felt to be safe for the treatment of morning sickness can also be used for motion sickness. These include the antihistamines meclizine and dimenhydrinate. (See 'Pregnant patients' above.)

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