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, clinical presentation, treatment and prevention of motion sickness. A possibly related disorder, disembarkment syndrome, and other causes of vertigo and dizziness are discussed separately. (See „Pathophysiology, etiology, and differential diagnosis 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, an illusory sense of motion, referred to as vection, can be evoked. This can sometimes result in motion sickness in the absence of physical movement.
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 . 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 . 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) .
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 . 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 . GABA also plays a role in motion sickness through effects on the velocity storage integrator .
RISK FACTORS — Motion sickness can be induced in almost all people with sufficient provocation. Individuals vary in their susceptibility to motion sickness, and certain characteristics show some correlation with this susceptibility.
- Sex — Women are generally more susceptible to motion sickness than men, but the incidence varies substantially with age .
- Age — Children less than two years old are typically resistant to motion sickness; the incidence peaks at approximately 12 years of age, and then decreases throughout adulthood.
- Hormonal factors — Pregnant women are particularly susceptible to motion sickness; susceptibility may also be affected by the menstrual cycle and by use of oral contraceptives [15,16].
- Other sensory illness — Diseases that alter vestibular or visual sensory cues (eg, labyrinthitis) may make subjects more sensitive to head motion and visual stimulation than the normal population. In addition, disorders that increase the sensitivity of the brain to sensory stimuli (eg, migraine) are associated with more prominent symptoms of motion sickness .
- Migraine — Migraine sufferers are more susceptible to motion sickness. In one study, 50 percent of migraine sufferers reported a history of motion sickness versus 20 percent of persons with tension headache . Symptoms of motion sickness in migraineurs may be movement or visually induced . A relationship between the trigeminal system and the vestibular nuclei may play a role in both migraine and motion sickness [20,21].
Reduced brain serotonin may be important in both motion sickness and migraine. In one study, migraine sufferers and control subjects were given an amino acid drink that contained or omitted L-tryptophan (required for the synthesis of serotonin) after which motion sickness was induced by the visual illusion of movement. Tryptophan depletion (reduced brain serotonin) resulted in increased symptoms of motion sickness in the control group to levels similar to that of the migraineurs . In a small randomized pilot study, rizatriptan, a triptan serotonin agonist, prevented the development of motion sickness symptoms in patients with migrainous vertigo .
- Psychosocial — Expectations and other psychological factors may affect the risk of motion sickness . A controlled trial found that naval cadets who were told they were unlikely to experience seasickness were at decreased risk of developing motion sickness .
- 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 .
- Body position — Lying supine, at least on a ship, may decrease susceptibility to motion sickness .
- Food — There are conflicting data on whether eating and drinking (and the type of food or drink) affect the risk of motion sickness [26,28-30].
INCIDENCE — Motion sickness can be induced in nearly all adults, so 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), 7 percent experienced vomiting, 21 percent felt „slightly unwell,“ 4 percent felt „quite ill,“ and 4 percent felt „absolutely dreadful“ .
- In a series of 923 passengers on 38 commercial airline flights, 0.5 percent reported vomiting, 8.4 percent reported nausea, and 16.2 percent reported illness .
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 (vection).
The principal symptoms are a nonvertiginous sense of dizziness, nausea, belching, increased salivation, warmth, and diaphoresis, and a general feeling of malaise [15,31]. The initial symptoms may be reported as a sense of being aware of one’s stomach. 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.
Motion sickness tends to improve or resolve with repeated exposure to the inciting stimulus . In a study of pilots undergoing flight simulator training, 47 percent of pilots reported motion sickness during their first flight and 24 percent during their last flight .
Symptoms typically subside after 36 to 72 hours of continuous exposure to a stimulus, but they can recur on returning to the pre-exposure environment (ie, returning to land after a sea voyage) .
TREATMENT AND PREVENTION — A number of interventions can be used to prevent or alleviate motion sickness . Treatments may be more effective when used for prevention rather than after symptoms have developed.
Environmental modification — Since conflicting sensory cues are believed to induce the symptoms of motion sickness, a straightforward treatment approach is to minimize the discrepancy between these cues. If visual and vestibular information are congruent, motion sickness is less likely to occur.
Labyrinthine cues cannot be readily manipulated, so this approach is based on providing visual information that contains equivalent motion information to that sensed by the vestibular system. Since the labyrinth senses motion in an inertial (earth-fixed) reference frame, this can be accomplished by viewing an earth-fixed environment during motion rather than a head-fixed environment. As an example, motion sickness on a ship is reduced if passengers view the horizon or land masses from the deck rather than their cabin. Similarly, passengers in a car should sit in the front seat and look through the window rather than sitting in the rear and focusing on an object moving with the interior of the car (such as a book).
Motion sickness does not occur during self-generated movements under normal conditions, so a second way to reduce the susceptibility to these symptoms is to control the motion of the vehicle. The driver of a car is less prone to motion sickness than a passenger, presumably because the driver’s brain can utilize the motor commands related to controlling the car to predict in an approximate manner the motion of the head.
Medication — Drug therapies can be used to suppress conflicting sensory cues in the brain regions that process afferent signals or to treat nausea. In general, the effectiveness of medications depends upon inhibition of activity in the vestibular nuclei, where labyrinthine and visual sensory cues are combined and synthesized. Drugs that reduce activity in the vestibular nuclei include antihistamines, anticholinergics, and benzodiazepines; other medications that reduce motion sickness include antidopaminergics and sympathomimetics (table 1) [15,35].
In general, medications should be taken before passive motion begins, since they are less effective in relieving symptoms that have already developed.
Antihistamines — A number of antihistamines can be used to treat motion sickness, and their effect is probably related to their anticholinergic effects . Medications include dimenhydrinate (Dramamine), diphenhydramine, chlorpheniramine , meclizine, cyclizine, and cinnarizine . Dimenhydrinate is available as a chewable tablet. Cinnarizine is not available in the United States, but is widely used in other countries.
Side effects are mainly related to anticholinergic effects and can include sedation, blurred vision, mouth dryness, and, in the elderly, 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 .
Nonsedating antihistamines do not appear to be effective for the treatment of motion sickness [39,40].
Anticholinergics — Scopolamine is commonly used for the management of motion sickness. A systematic review of randomized trials concluded that scopolamine is effective for prevention of motion sickness, but that no trials had examined its effectiveness in treating established motion sickness, and that the evidence comparing scopolamine with other treatments was inadequate .
At least three randomized trials were performed after the systematic review:
- In a trial of experimentally induced motion sickness in 75 patients, scopolamine was more effective in preventing motion sickness than promethazine,meclizine, and lorazepam .
- In a trial of the prevention of seasickness in 76 naval crew members, scopolamine was more effective than cinnarizine, an antihistamine . Although differences were marginally significant, scopolamine was associated with fewer adverse effects than cinnarizine.
- In a trial of preventing motion sickness in 64 helicopter passengers, the combination of promethazine and caffeine appeared to be more effective thanscopolamine alone .
Scopolamine is most commonly administered as a transdermal patch applied every 72 hours. Side effects include those discussed above (sedation, blurred vision, mouth dryness, and, in older adults, confusion and urinary retention), and scopolamine is contraindicated in people at risk for angle closure glaucoma. Some instances of poor clinical response to scopolamine patches may be due to inadequate transdermal absorption leading to inappropriately low scopolamine levels in the blood .
Antidopaminergics — Promethazine can be used both for prevention and treatment of motion sickness [15,45]. In two trials of the prevention of motion sickness cited above, promethazine appeared to be less effective than scopolamine but more effective than meclizine or lorazepam , and promethazine and caffeine appeared to be more effective than scopolamine .
Side effects of antidopaminergics include sedation and extrapyramidal effects.
Sympathomimetics — Ephedrine and amphetamines have been used both to treat motion sickness and to counteract the sedating effects of other medications . (See ‚Effect on performance‘ below.) Ephedrine may have some benefit even after symptoms have developed . Amphetamines are controlled substances with potentially significant side effects and the potential for addiction. Although less studied, pseudoephedrine is readily available in the United States including in combination medications with sedating antihistamines.
Caffeine may also be of benefit when used in combination with other medications. A randomized trial in 64 patients examined the effects of promethazine 25 mg plus caffeine 200 mg, meclizine 25 mg, scopolamine patch 1.5 mg, and an acustimulation wristband . Only the combination of promethazine and caffeine produced a significant decrease in symptoms; the combination also improved reaction times.
- Benzodiazepines may be of some benefit for motion sickness, but they are sedating .
- Standard antiemetics such as prochlorperazine or ondansetron can relieve nausea, which is usually the most prominent symptom of motion sickness . However, in two studies in highly susceptible subjects, one in a laboratory model of simulated rotation and one at sea, ondansetron was ineffective in preventing motion sickness [50,51]. (See „Migrainous vertigo“, section on ‚Treatment‘.)
- GABA agonists such as baclofen or gabapentin inhibit the „velocity storage“ mechanism in the central vestibular system that may be specifically responsible for producing motion sickness. The utility of these drugs has not been extensively studied to date and their potential usefulness is currently based on results from experiments that use complex movements to induce motion sickness and on case reports [10,11].
Effect on performance — Treating 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 most of the medications used are sedating [52,53].
Dimenhydrinate may have particularly negative effects on performance . A controlled trial of medications for experimental motion sickness in 67 adults suggested that, at clinically useful doses, the drugs had the following order from best to worst for cognitive side effects: meclizine, scopolamine, promethazine, lorazepam .
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 . Another trial found that ephedrine decreased sleepiness and improved performance in patients administeredchlorpheniramine, although it did not add to the effectiveness of chlorpheniramine in treating motion sickness .
Treatment in pregnancy — As mentioned above, pregnant women 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, diphenhydramine, and dimenhydrinate), andprochlorperazine, which is listed as category C in pregnancy by the US Food and Drug Administration (FDA) (table 2). (See „Clinical features and evaluation of nausea and vomiting of pregnancy“.)
Physical therapy — As discussed above, the vestibular response to head motion can decline over time (habituate), if a given motion pattern is presented repetitively. For this reason, physical therapy approaches that utilize recurrent head movements and associated visual cues can sometimes reduce the sensitivity to motion sickness in subjects who are particularly prone to this problem.
Ginger — Ginger has been used as an alternative medicine to prevent motion sickness. Randomized trials both in experimental motion sickness and in naval cadets at sea have found benefit with pretreatment with one to two grams of ginger [58,59]. The mechanism of benefit with ginger appears to be related to its effects on gastric motility rather than the vestibular system [60,61].
Acupressure — 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 has been reported to be effective for motion sickness in some [62-64], but not all [65-67], controlled trials. A randomized trial with a device that applies electrical stimulation to the P6 point found no benefit .
While these results raise the possibility that acupressure may be of benefit for motion sickness, trials of this sort can be difficult to perform with adequate blinding and allocation concealment. It remains uncertain whether acupressure is effective.
Magnets — Although sometimes promoted for this use, we know of no studies evaluating the efficacy of magnets in the treatment of motion sickness.
Nicotine deprivation — One small observational study found that overnight nicotine deprivation in smokers resulted in a reduction in motion sickness susceptibility . The effect was most pronounced in subjects who were heavy smokers and with mild to moderate susceptibility to motion sickness.
INFORMATION FOR PATIENTS
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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 information: Motion sickness (The Basics)“)
SUMMARY AND RECOMMENDATIONS
- Motion sickness is believed to be caused by conflicts between sensory cues regarding perceived motion.
- Nearly everyone will develop motion sickness with a sufficient stimulus; however, individual susceptibility to motion sickness is variable.
- Symptoms include a nonvertiginous sense of dizziness, nausea, belching, increased salivation, warmth, diaphoresis, and a general feeling of malaise. With continuous exposure to a stimulus, symptoms typically subside over 36 to 72 hours.
- Individuals can prevent or treat motion sickness by keeping visual cues congruous with vestibular cues. This can be achieved by looking at the outside world’s frame of reference (ie, sit in the front seat and look out the front window in a car or view the horizon from the deck of a ship). Activities that maintain vision within a local frame of reference are particularly provocative for motion sickness (eg, reading a book or watching a video or movie). Self-generated movements do not induce motion sickness, and controlling the motion of a vehicle (eg, driving) reduces the likelihood of motion sickness. Lying supine can decrease motion sickness.
- Medications with anticholinergic effects (including sedating antihistamines) are most commonly used for treatment of motion sickness; nonsedating antihistamines are not effective. Meclizine is probably less sedating than dimenhydrinate or diphenhydramine at an equally effective dose; as a result, the choice of antihistamine can be based in part on whether or not sedation is desired. Transdermal scopolamine is effective, and a patch can be worn continuously for 72 hours. Caution must be taken when using medications with anticholinergic effects in the elderly or in patients at risk for angle closure glaucoma. Other medications can also be used (table 1).
- Alternative treatments are often considered for motion sickness. Randomized trials suggest that one to two grams of ginger may help prevent motion sickness. There is conflicting evidence on acupressure, but acupressure is safer than many other treatments, and some patients report finding it helpful.
Common pharmacologic therapies for motion sickness
- Promethazine (Anergan, Phenergan)
- Scopolamine (Transderm-Scop)
- Cyclizine (Marezine)
- Buclizine (Bucladin-S Softabs)
Drug ratings in pregnancy (US Food & Drug Administration)
|A||Controlled human studies show no risk|
|Controlled studies in pregnant women fail to demonstrate a risk to the fetus in the first trimester with no evidence of risk in later trimesters. The possibility of fetal harm appears remote.|
|B||No evidence of risk in studies|
|Either animal-reproduction studies have not demonstrated a fetal risk but there are no controlled studies in pregnant women, or animal-reproduction studies have shown an adverse effect (other than a decrease in fertility) that was not confirmed in controlled studies in women in the first trimester and there is no evidence of a risk in later trimesters.|
|C||Risk cannot be ruled out|
|Either studies in animals have revealed adverse effects on the fetus (teratogenic or embryocidal effects or other) and there are no controlled studies in women, or studies in women and animals are not available. Drugs should be given only if the potential benefits justify the potential risk to the fetus.|
|D||Positive evidence of risk|
|There is positive evidence of human fetal risk, but the benefits from use in pregnant women may be acceptable despite the risk (eg, if the drug is needed in a life-threatening situation or for a serious disease for which safer drugs cannot be used or are ineffective).|
|X||Contraindicated in pregnancy|
|Studies in animals or human beings have demonstrated fetal abnormalities or there is evidence of fetal risk based on human experience, or both, and the risk of the use of the drug in pregnant women clearly outweighs any possible benefit. The drug is contraindicated in women who are or may become pregnant.|
P6 acupressure point
Pressure or massage at the P6 acupressure point is reported in some studies to relieve motion sickness. The point is found three of the patient’s fingerbreadths proximal to the proximal wrist fold, between the palmaris longus and flexor carpi radialis tendons, shown in this picture by the tip of the pen.
- Oman CM. Motion sickness: a synthesis and evaluation of the sensory conflict theory. Can J Physiol Pharmacol 1990; 68:294.
- Flanagan MB, May JG, Dobie TG. The role of vection, eye movements and postural instability in the etiology of motion sickness. J Vestib Res 2004; 14:335.
- Shupak A, Gordon CR. Motion sickness: advances in pathogenesis, prediction, prevention, and treatment. Aviat Space Environ Med 2006; 77:1213.
- Miller EF 2nd, Graybiel A. Semicircular canals as a primary etiological factor in motion sickness. Aerosp Med 1972; 43:1065.
- Brizzee KR, Igarashi M. Effect of macular ablation on frequency and latency of motion-induced emesis in the squirrel monkey. Aviat Space Environ Med 1986; 57:1066.
- James W. The sense of dizziness in deaf-mutes. Am J Otol 1882; 4:239.
- Graybiel A. Susceptibility to acute motion sickness in blind persons. Aerosp Med 1970; 41:650.
- Woodman PD, Griffin MJ. Effect of direction of head movement on motion sickness caused by Coriolis stimulation. Aviat Space Environ Med 1997; 68:93.
- Balaban CD, Porter JD. Neuroanatomic substrates for vestibulo-autonomic interactions. J Vestib Res 1998; 8:7.
- Dai M, Kunin M, Raphan T, Cohen B. The relation of motion sickness to the spatial-temporal properties of velocity storage. Exp Brain Res 2003; 151:173.
- Cohen B, Dai M, Raphan T. The critical role of velocity storage in production of motion sickness. Ann N Y Acad Sci 2003; 1004:359.
- Takeda N, Morita M, Hasegawa S, et al. Neuropharmacology of motion sickness and emesis. A review. Acta Otolaryngol Suppl 1993; 501:10.
- Cohen B, Dai M, Yakushin SB, Raphan T. Baclofen, motion sickness susceptibility and the neural basis for velocity storage. Prog Brain Res 2008; 171:543.
- Cooper C, Dunbar N, Mira M. Sex and seasickness on the Coral Sea. Lancet 1997; 350:892.
- Gahlinger PM. Motion sickness. How to help your patients avoid travel travail. Postgrad Med 1999; 106:177.
- Grunfeld E, Gresty MA. Relationship between motion sickness, migraine and menstruation in crew members of a „round the world“ yacht race. Brain Res Bull 1998; 47:433.
- Barabas G, Matthews WS, Ferrari M. Childhood migraine and motion sickness. Pediatrics 1983; 72:188.
- Kayan A, Hood JD. Neuro-otological manifestations of migraine. Brain 1984; 107 ( Pt 4):1123.
- Drummond PD. Triggers of motion sickness in migraine sufferers. Headache 2005; 45:653.
- Marcus DA, Furman JM, Balaban CD. Motion sickness in migraine sufferers. Expert Opin Pharmacother 2005; 6:2691.
- Drummond PD, Granston A. Facial pain increases nausea and headache during motion sickness in migraine sufferers. Brain 2004; 127:526.
- Drummond PD. Effect of tryptophan depletion on symptoms of motion sickness in migraineurs. Neurology 2005; 65:620.
- Marcus DA, Furman JM. Prevention of motion sickness with rizatriptan: a double-blind, placebo-controlled pilot study. Med Sci Monit 2006; 12:PI1.
- Murray JB. Psychophysiological aspects of motion sickness. Percept Mot Skills 1997; 85:1163.
- Eden D, Zuk Y. Seasickness as a self-fulfilling prophecy: raising self-efficacy to boost performance at sea. J Appl Psychol 1995; 80:628.
- Turner M, Griffin MJ, Holland I. Airsickness and aircraft motion during short-haul flights. Aviat Space Environ Med 2000; 71:1181.
- Gahlinger PM. Cabin location and the likelihood of motion sickness in cruise ship passengers. J Travel Med 2000; 7:120.
- Lawther A, Griffin MJ. A survey of the occurrence of motion sickness amongst passengers at sea. Aviat Space Environ Med 1988; 59:399.
- Lindseth G, Lindseth PD. The relationship of diet to airsickness. Aviat Space Environ Med 1995; 66:537.
- Hu S, Lagomarsino JJ, Luo YJ. Drinking milk or water has no effect on the severity of optokinetic rotation-induced symptoms of motion sickness. Aviat Space Environ Med 1998; 69:1158.
- Money KE. Motion sickness. Physiol Rev 1970; 50:1.
- Spinks AB, Wasiak J, Villanueva EV, Bernath V. Scopolamine (hyoscine) for preventing and treating motion sickness. Cochrane Database Syst Rev 2007; :CD002851.
- Ungs TJ. Simulator induced syndrome in Coast Guard aviators. Aviat Space Environ Med 1988; 59:267.
- Murdin L, Golding J, Bronstein A. Managing motion sickness. BMJ 2011; 343:d7430.
- Brandt T, Dichgans J, Wagner W. Drug effectiveness on experimental optokinetic and vestibular motion sickness. Aerosp Med 1974; 45:1291.
- Buckey JC, Alvarenga D, Cole B, Rigas JR. Chlorpheniramine for motion sickness. J Vestib Res 2004; 14:53.
- Lucertini M, Mirante N, Casagrande M, et al. The effect of cinnarizine and cocculus indicus on simulator sickness. Physiol Behav 2007; 91:180.
- Weinstein SE, Stern RM. Comparison of marezine and dramamine in preventing symptoms of motion sickness. Aviat Space Environ Med 1997; 68:890.
- Kohl RL, Homick JL, Cintron N, Calkins DS. Lack of effects of astemizole on vestibular ocular reflex, motion sickness, and cognitive performance in man. Aviat Space Environ Med 1987; 58:1171.
- Cheung BS, Heskin R, Hofer KD. Failure of cetirizine and fexofenadine to prevent motion sickness. Ann Pharmacother 2003; 37:173.
- Dornhoffer J, Chelonis JJ, Blake D. Stimulation of the semicircular canals via the rotary chair as a means to test pharmacologic countermeasures for space motion sickness. Otol Neurotol 2004; 25:740.
- Gil A, Nachum Z, Tal D, Shupak A. A comparison of cinnarizine and transdermal scopolamine for the prevention of seasickness in naval crew: a double-blind, randomized, crossover study. Clin Neuropharmacol 2012; 35:37.
- Estrada A, LeDuc PA, Curry IP, et al. Airsickness prevention in helicopter passengers. Aviat Space Environ Med 2007; 78:408.
- Gil A, Nachum Z, Dachir S, et al. Scopolamine patch to prevent seasickness: clinical response vs. plasma concentration in sailors. Aviat Space Environ Med 2005; 76:766.
- Davis JR, Jennings RT, Beck BG, Bagian JP. Treatment efficacy of intramuscular promethazine for space motion sickness. Aviat Space Environ Med 1993; 64:230.
- Kohl RL. Failure of metoclopramide to control emesis or nausea due to stressful angular or linear acceleration. Aviat Space Environ Med 1987; 58:125.
- Wood CD, Stewart JJ, Wood MJ, et al. Therapeutic effects of antimotion sickness medications on the secondary symptoms of motion sickness. Aviat Space Environ Med 1990; 61:157.
- McClure JA, Lycett P, Baskerville JC. Diazepam as an anti-motion sickness drug. J Otolaryngol 1982; 11:253.
- Benline TA, French J, Poole E. Anti-emetic drug effects on pilot performance: granisetron vs. ondansetron. Aviat Space Environ Med 1997; 68:998.
- Muth ER, Elkins AN. High dose ondansetron for reducing motion sickness in highly susceptible subjects. Aviat Space Environ Med 2007; 78:686.
- Hershkovitz D, Asna N, Shupak A, et al. Ondansetron for the prevention of seasickness in susceptible sailors: an evaluation at sea. Aviat Space Environ Med 2009; 80:643.
- Nicholson AN, Stone BM, Turner C, Mills SL. Central effects of cinnarizine: restricted use in aircrew. Aviat Space Environ Med 2002; 73:570.
- Cowings PS, Toscano WB, DeRoshia C, Miller NE. Promethazine as a motion sickness treatment: impact on human performance and mood states. Aviat Space Environ Med 2000; 71:1013.
- Gordon CR, Gonen A, Nachum Z, et al. The effects of dimenhydrinate, cinnarizine and transdermal scopolamine on performance. J Psychopharmacol 2001; 15:167.
- Paule MG, Chelonis JJ, Blake DJ, Dornhoffer JL. Effects of drug countermeasures for space motion sickness on working memory in humans. Neurotoxicol Teratol 2004; 26:825.
- Paul MA, MacLellan M, Gray G. Motion-sickness medications for aircrew: impact on psychomotor performance. Aviat Space Environ Med 2005; 76:560.
- Buckey JC Jr, Alvarenga DL, MacKenzie TA. Chlorpheniramine and ephedrine in combination for motion sickness. J Vestib Res 2007; 17:301.
- Grøntved A, Brask T, Kambskard J, Hentzer E. Ginger root against seasickness. A controlled trial on the open sea. Acta Otolaryngol 1988; 105:45.
- 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 Physiol Gastrointest Liver Physiol 2003; 284:G481.
- Holtmann S, Clarke AH, Scherer H, Höhn M. The anti-motion sickness mechanism of ginger. A comparative study with placebo and dimenhydrinate. Acta Otolaryngol 1989; 108:168.
- Ghayur MN, Gilani AH. Pharmacological basis for the medicinal use of ginger in gastrointestinal disorders. Dig Dis Sci 2005; 50:1889.
- Hu S, Stritzel R, Chandler A, Stern RM. P6 acupressure reduces symptoms of vection-induced motion sickness. Aviat Space Environ Med 1995; 66:631.
- Stern RM, Jokerst MD, Muth ER, Hollis C. Acupressure relieves the symptoms of motion sickness and reduces abnormal gastric activity. Altern Ther Health Med 2001; 7:91.
- Bertalanffy P, Hoerauf K, Fleischhackl R, et al. Korean hand acupressure for motion sickness in prehospital trauma care: a prospective, randomized, double-blinded trial in a geriatric population. Anesth Analg 2004; 98:220.
- Bruce DG, Golding JF, Hockenhull N, Pethybridge RJ. Acupressure and motion sickness. Aviat Space Environ Med 1990; 61:361.
- Warwick-Evans LA, Masters IJ, Redstone SB. A double-blind placebo controlled evaluation of acupressure in the treatment of motion sickness. Aviat Space Environ Med 1991; 62:776.
- Miller KE, Muth ER. Efficacy of acupressure and acustimulation bands for the prevention of motion sickness. Aviat Space Environ Med 2004; 75:227.
- Golding JF, Prosyanikova O, Flynn M, Gresty MA. The effect of smoking nicotine tobacco versus smoking deprivation on motion sickness. Auton Neurosci 2011; 160:53.