Motion sickness

Motion sickness occurs due to a difference between actual and expected motion.[1] Symptoms commonly include nausea, vomiting, cold sweat, headache, sleepiness, yawning, loss of appetite, and increased salivation.[1] Complications may rarely include dehydration, electrolyte problems, or a lower esophageal tear.[1]

Motion sickness
Other namesKinetosis, travel sickness, seasickness, airsickness, carsickness, simulation sickness, space motion sickness, space adaptation syndrome
A drawing of people with sea sickness from 1841
SpecialtyNeurology
SymptomsNausea, vomiting, cold sweat, increased salivation[1]
ComplicationsDehydration, electrolyte problems, lower esophageal tear[1]
CausesReal or perceived motion[1]
Risk factorsPregnancy, migraines, Meniere’s disease[1]
Diagnostic methodBased on symptoms[1]
Differential diagnosisBenign paroxysmal positional vertigo, vestibular migraine, stroke[1]
PreventionAvoidance of triggers[1]
TreatmentBehavioral measures, medications[2]
MedicationScapolamine, dimenhydrinate, dexamphetamine[2]
PrognosisGenerally resolve within a day[1]
FrequencyNearly all people with sufficient motion[2]

The cause of motion sickness is either real or perceived motion.[1] This may include from car travel, air travel, sea travel, space travel, or reality simulation.[1] Risk factors include pregnancy, migraines, and Meniere’s disease.[1] The diagnosis is based on symptoms.[1]

Treatment may include behavioral measures or medications.[2] Behavioral measures include keeping the head still and focusing on the horizon.[1] Three type of medications are useful: antimuscarinics such as scopolamine, H1 antihistamines such as dimenhydrinate, and amphetamines such as dexamphetamine.[2] Side effects, however, may limit the use of medications.[2] A number of medications used for nausea such as ondansetron are not effective for motion sickness.[2]

Nearly all people are affected with sufficient motion.[1] Susceptibility, however, is variable.[1] Women are more easily affected than men.[1] Motion sickness has been described since at least the time of Hippocrates.[1] "Nausea" is from the Greek naus meaning ship.[1]

Signs and symptoms

Symptoms commonly include nausea, vomiting, cold sweat, headache, sleepiness, yawning, loss of appetite, and increased salivation.[1] Occasionally tiredness can last for hours to days an episode of motion sickness, known as "sopite syndrome".[1] Rarely severe symptoms such as the inability to walk, ongoing vomiting, or social isolation may occur.[1]

Cause

Motion sickness can be divided into three categories:

  1. Motion sickness caused by motion that is felt but not seen, as in terrestrial motion sickness;
  2. Motion sickness caused by motion that is seen but not felt, as in space motion sickness;
  3. Motion sickness caused when both systems detect motion but they do not correspond, as in either terrestrial or space motion sickness.

Motion felt but not seen

In these cases, motion is sensed by the vestibular system and hence the motion is felt, but no motion or little motion is detected by the visual system, as in terrestrial motion sickness.

Carsickness

A specific form of terrestrial motion sickness, being carsick is quite common and evidenced by disorientation while reading a map, a book, or a small screen during travel. Carsickness results from the sensory conflict arising in the brain from differing sensory inputs. Motion sickness is caused by a conflict between signals arriving in the brain from the inner ear, which forms the base of the vestibular system, the sensory apparatus that deals with movement and balance, and which detects motion mechanically. If someone is looking at a stationary object within a vehicle, such as a magazine, their eyes will inform their brain that what they are viewing is not moving. Their inner ears, however, will contradict this by sensing the motion of the vehicle.[3] Varying theories exist as to cause. The sensory conflict theory notes that the eyes view motion while riding in the moving vehicle while other body sensors sense stillness, creating conflict between the eyes and inner ear. Another suggests the eyes mostly see the interior of the car which is motionless while the vestibular system of the inner ear senses motion as the vehicle goes around corners or over hills and even small bumps. Therefore, the effect is worse when looking down but may be lessened by looking outside of the vehicle.

In the early 20th century, Austro-Hungarian scientist Robert Barany observed the back and forth movement of the eyes of railroad passengers as they looked out the side windows at the scenery whipping by. He called it "railway nystagmus". Also called "optokinetic nystagmus". It causes nausea and vomiting. His findings were published in the journal Laeger, 83:1516, Nov.17, 1921.

Airsickness

Air sickness is a kind of terrestrial motion sickness induced by certain sensations of air travel.[4] It is a specific form of motion sickness and is considered a normal response in healthy individuals. It is essentially the same as carsickness but occurs in an airplane. An airplane may bank and tilt sharply, and unless passengers are sitting by a window, they are likely to see only the stationary interior of the plane due to the small window sizes and during flights at night. Another factor is that while in flight, the view out of windows may be blocked by clouds, preventing passengers from seeing the moving ground or passing clouds.

Seasickness

Seasickness is a form of terrestrial motion sickness characterized by a feeling of nausea and, in extreme cases, vertigo experienced after spending time on a boat.[4] It is essentially the same as carsickness, though the motion of a watercraft tends to be more regular. It is typically brought on by the rocking motion of the craft[5][6] or movement while the craft is immersed in water.[7] As with airsickness, it can be difficult to visually detect motion even if one looks outside the boat since water does not offer fixed points with which to visually judge motion. Poor visibility conditions, such as fog, may worsen seasickness. The greatest contributor to seasickness is the tendency for people being affected by the rolling or surging motions of the craft to seek refuge below decks, where they are unable to relate themselves to the boat's surroundings and consequent motion. Some sufferers of carsickness are resistant to seasickness and vice versa. Adjusting to the craft's motion at sea is called "gaining one's sea legs"; it can take a significant portion of the time spent at sea after disembarking to regain a sense of stability "post-sea legs".

Centrifuge motion sickness

Rotating devices such as centrifuges used in astronaut training and amusement park rides such as the Rotor, Mission: Space and the Gravitron can cause motion sickness in many people. While the interior of the centrifuge does not appear to move, one will experience a sense of motion. In addition, centrifugal force can cause the vestibular system to give one the sense that downward is in the direction away from the center of the centrifuge rather than the true downward direction.

Dizziness due to spinning

When one spins and stops suddenly, fluid in the inner ear continues to rotate causing a sense of continued spinning while one's visual system no longer detects motion.

Virtual reality

Usually, VR programs would detect the motion of the user's head and abject the rotation of vision to avoid dizziness. However, some cases such as system lagging or software crashing could cause lags in the screen updates. In such cases, even some small head motions could trigger the motion sickness by the defense mechanism that mentioned above: The inner ear transmits to the brain that it senses motion, but the eyes tell the brain that everything is still. As a result of the incongruity, the brain concludes that the individual is hallucinating and further concludes that the hallucination is due to poison ingestion. The brain responds by inducing vomiting, to clear the supposed toxin.[8]

Motion seen but not felt

In these cases, motion is detected by the visual system and hence the motion is seen, but no motion or little motion is sensed by the vestibular system. Motion sickness arising from such situations has been referred to as "visually induced motion sickness" (VIMS).[9]

Space motion sickness

Zero gravity interferes with the vestibular system's gravity-dependent operations, so that the two systems, vestibular and visual, no longer provide a unified and coherent sensory representation. This causes unpleasant disorientation sensations often quite distinct from terrestrial motion sickness, but with similar symptoms. The symptoms may be more intense because a condition caused by prolonged weightlessness is usually quite unfamiliar.

Space motion sickness was effectively unknown during the earliest spaceflights because the very cramped conditions of the spacecraft allowed for only minimal bodily motion, especially head motion. Space motion sickness seems to be aggravated by being able to freely move around, and so is more common in larger spacecraft.[4] Around 60% of Space Shuttle astronauts currently experience it on their first flight; the first case of space motion sickness is now thought to be the Soviet cosmonaut Gherman Titov, in August 1961 onboard Vostok 2, who reported dizziness, nausea, and vomiting. The first severe cases were in early Apollo flights; Frank Borman on Apollo 8 and Rusty Schweickart on Apollo 9. Both experienced identifiable and quite unpleasant symptoms-—in the latter case causing the mission plan to be modified.

Screen images

This type of terrestrial motion sickness is particularly prevalent when susceptible people are watching films presented on very large screens such as IMAX, but may also occur in regular format theaters or even when watching TV or playing games. For the sake of novelty, IMAX and other panoramic type theaters often show dramatic motions such as flying over a landscape or riding a roller coaster. This type of motion sickness can be prevented by closing one's eyes during such scenes.

In regular-format theaters, an example of a movie that caused motion sickness in many people is The Blair Witch Project. Theaters warned patrons of its possible nauseating effects, cautioning pregnant women in particular. Blair Witch was filmed with a handheld camcorder, which was subjected to considerably more motion than the average movie camera,[10] and lacks the stabilization mechanisms of steadicams.

Home movies, often filmed with a cell phone camera, also tend to cause motion sickness in those who view them. The person holding the cell phone or other camera usually is unaware of this as the recording is being made since the sense of motion seems to match the motion seen through the camera's viewfinder. Those who view the film afterward only see the movement, which may be considerable, without any sense of motion. Using the zoom function seems to contribute to motion sickness as well since zooming is not a normal function of the eye. The use of a tripod or a camera or cell phone with image stabilization while filming can reduce this effect.

Virtual reality

Motion sickness due to virtual reality is very similar to simulation sickness and motion sickness due to films.[11] In virtual reality the effect is made more acute as all external reference points are blocked from vision, the simulated images are three-dimensional and in some cases stereo sound that may also give a sense of motion. The NADS-1, a simulator located at the National Advanced Driving Simulator, is capable of accurately stimulating the vestibular system with a 360-degree horizontal field of view and 13 degrees of freedom motion base.[12] Studies have shown that exposure to rotational motions in a virtual environment can cause significant increases in nausea and other symptoms of motion sickness.[13]

In a study conducted by the U.S. Army Research Institute for the Behavioral and Social Sciences in a report published May 1995 titled "Technical Report 1027 - Simulator Sickness in Virtual Environments", out of 742 pilot exposures from 11 military flight simulators, "approximately half of the pilots (334) reported post-effects of some kind: 250 (34%) reported that symptoms dissipated in less than one hour, 44 (6%) reported that symptoms lasted longer than four hours, and 28 (4%) reported that symptoms lasted longer than six hours. There were also four (1%) reported cases of spontaneously occurring flashbacks."[14]

Motion that is seen and felt

When moving within a rotating reference frame such as in a centrifuge or environment where gravity is simulated with centrifugal force, the coriolis effect causes a sense of motion in the vestibular system that does not match the motion that is seen.

Pathophysiology

There are various theories that attempt to explain the cause of the condition.

Sensory conflict theory

At present a "fully adequate theory of motion sickness is not presently available" but contemporary sensory conflict theory, referring to "a discontinuity between either visual, proprioceptive, and somatosensory input, or semicircular canal and otolith input", is probably the most thoroughly studied.[15] According to this theory, when the brain presents the mind with two incongruous states of motion; the result is often nausea and other symptoms of disorientation known as motion sickness. Such conditions happen when the vestibular system and the visual system do not present a synchronized and unified representation of one's body and surroundings.

According to sensory conflict theory, the cause of terrestrial motion sickness is the opposite of the cause of space motion sickness. The former occurs when one perceives visually that one's surroundings are relatively immobile while the vestibular system reports that one's body is in motion relative to its surroundings.[4] The latter can occur when the visual system perceives that one's surroundings are in motion while the vestibular system reports relative bodily immobility (as in zero gravity.)

Neural mismatch

A variation of the sensory conflict theory is known as neural mismatch, implying a mismatch occurring between ongoing sensory experience and long-term memory rather than between components of the vestibular and visual systems. This theory emphasizes "the limbic system in the integration of sensory information and long-term memory, in the expression of the symptoms of motion sickness, and the impact of anti-motion-sickness drugs and stress hormones on limbic system function. The limbic system may be the neural mismatch center of the brain."[16]

Defense against poisoning

A very different alternate is the defense mechanism theory holding that motion sickness functions as a defense mechanism against neurotoxins.[17] The area postrema in the brain is responsible for inducing vomiting when poisons are detected, and for resolving conflicts between vision and balance. When feeling motion but not seeing it (for example, in the cabin of a ship with no portholes), the inner ear transmits to the brain that it senses motion, but the eyes tell the brain that everything is still. As a result of the incongruity, the brain concludes that the individual is hallucinating and further concludes that the hallucination is due to poison ingestion. The brain responds by inducing vomiting, to clear the supposed toxin. Treisman's indirect argument has recently been questioned via an alternative direct evolutionary hypothesis, as well as modified and extended via a direct poison hypothesis.[8] The direct evolutionary hypothesis essentially argues that there are plausible means by which ancient real or apparent motion could have contributed directly to the evolution of aversive reactions, without the need for the co-opting of a poison response as posited by Treisman. Nevertheless, the direct poison hypothesis argues that there still are plausible ways in which the body's poison response system may have played a role in shaping the evolution of some of the signature symptoms that characterize motion sickness.

Nystagmus hypothesis

Yet another theory, known as the nystagmus hypothesis,[18] has been proposed based on stimulation of the vagus nerve resulting from the stretching or traction of extra-ocular muscles co-occurring with eye movements caused by vestibular stimulation. There are three critical aspects to the theory: first is the close linkage between activity in the vestibular system, i.e., semicircular canals and otolith organs, and a change in tonus among various of each eye's six extra-ocular muscles. Thus, with the exception of voluntary eye movements, the vestibular and oculomotor systems are thoroughly linked. Second is the operation of Sherrington's Law[19] describing reciprocal inhibition between agonist-antagonist muscle pairs, and by implication the stretching of extraocular muscle that must occur whenever Sherrington's Law is made to fail, thereby causing an unrelaxed (contracted) muscle to be stretched. Finally, there is the critical presence of afferent output to the Vagus nerves as a direct result of eye muscle stretch or traction.[20] Thus, 10th nerve stimulation resulting from eye muscle stretch is proposed as the cause of motion sickness. The theory explains why labyrinthine-defective individuals are immune to motion sickness;[21][22] why symptoms emerge when undergoing various body-head accelerations; why combinations of voluntary and reflexive eye movements may challenge the proper operation of Sherrington's Law, and why many drugs that suppress eye movements also serve to suppress motion sickness symptoms.[23]

A recent theory [24] argues that the main reason motion sickness occurs is due to an imbalance in vestibular outputs favoring the semicircular canals (nauseogenic) vs. otolith organs (anti-nauseogenic). This theory attempts to integrate previous theories of motion sickness. For example, there are many sensory conflicts that are associated with motion sickness and many that are not, but those in which canal stimulation occurs in the absence of normal otolith function (e.g., 0-g) are the most provocative. The vestibular imbalance theory is also tied to the different roles of the otoliths and canals in autonomic arousal (otolith output more sympathetic).

Diagnosis

The diagnosis is based on symptoms.[1] Other conditions that may present similarly include vestibular disorders such as benign paroxysmal positional vertigo and vestibular migraine and stroke.[1]

Treatment

Treatment may include behavioral measures or medications.[2]

Behavioral measures

Behavioral measures to decrease motion sickness include holding the head still and lying on the back.[2] Focusing on the horizon may also be useful.[1] Listening to music, mindful breathing, being the driver, and not reading while moving are other techniques.[1]

Habituation is the most effective technique but requires significant time.[1] It is often used by the military for pilots.[1] These techniques must be carried out at least every week to retain effectiveness.[1]

A head-worn, computer device with a transparent display can be used to mitigate the effects of motion sickness (and spatial disorientation) if visual indicators of the wearer’s head position are shown.[25] Such a device functions by providing the wearer with digital reference lines in their field of vision that indicate the horizon’s position relative to the user’s head. This is accomplished by combining readings from accelerometers and gyroscopes mounted in the device. This technology has been implemented in both standalone devices[26] and Google Glass.[27][28] In two NIH-backed studies, greater than 90% of people experienced a reduction in the symptoms of motion sickness while using this technology.[25] One promising looking treatment is for to wear LCD shutter glasses that create a stroboscopic vision of 4 Hz with a dwell of 10 milliseconds.[29]

Medication

Three types of medications are useful: antimuscarinics such as scopolamine, H1 antihistamines such as dimenhydrinate, and amphetamines such as dexamphetamine.[2] Benefits are greater if used before the onset of simple or shortly after symptoms begin.[1] Side effects, however, may limit the use of medications.[2] A number of medications used for nausea such as ondansetron and metoclopramide are not effective in motion sickness.[2][1]

Scopolamine is the most effective medication.[1] Evidence is best for when it is used preventatively.[30] It is available as a skin patch.[1] Side effects may include blurry vision.[1]

Others effective first generation antihistamines include meclizine, promethazine, cyclizine, and cinnarizine.[1] In pregnancy meclizine and dimenhydrinate are generally felt to be safe.[1] Side effects include sleepiness.[1] Second generation antihistamines have not been found to be useful.[1]

Dextroamphetamine may be used together with an antihistamine or an antimuscarinic.[1] Concerns include their addictive potential.[1]

Those involved in high-risk activities, such as SCUBA diving, should evaluate the risks versus the benefits of medications.[31][32][33][34][35] Promethazine combined with ephedrine to counteract the sedation is known as "the Coast Guard cocktail".[36]

Alternative medicine

Acupuncture has not been found to be useful.[2] Ginger root is commonly thought to be an effective anti-emetic, but it is ineffective in treating motion sickness.[37] Providing smells does not appear to have a significant effect on the rate of motion sickness.[2]

Epidemiology

Roughly one-third of people are highly susceptible to motion sickness, and most of the rest get motion sick under extreme conditions. The rates of space motion sickness has been estimated at between forty and eighty percent of those who enter weightless orbit. Several factors influence susceptibility to motion sickness, including sleep deprivation and the cubic footage allocated to each space traveler. Studies indicate that women are more likely to be affected than men,[38] and that the risk decreases with advancing age. There is some evidence that people with Asian ancestry may develop motion sickness more frequently than people of European ancestry, and there are situational and behavioral factors, such as whether a passenger has a view of the road ahead, and diet and eating behaviors.[39]

References

  1. Takov, V; Tadi, P (January 2019). "Motion Sickness". PMID 30969528. Cite journal requires |journal= (help)
  2. Golding, J. F. (2016). "Motion sickness". Handbook of Clinical Neurology. 137: 371–390. doi:10.1016/B978-0-444-63437-5.00027-3. ISBN 9780444634375. ISSN 0072-9752. PMID 27638085.
  3. "Preventing passengers in autonomous cars from feeling queasy". The Economist. 2018-02-01. Retrieved 2018-02-05.
  4. Benson, Alan J. (2002). "Motion Sickness" (PDF). In Kent B. Pandoff; Robert E. Burr (eds.). Medical Aspects of Harsh Environments. 2. Washington, D.C.: Borden Institute. pp. 1048–1083. ISBN 978-0-16-051184-4. Retrieved 27 Mar 2017.
  5. Gahlinger, P. M. (2000). "A comparison of motion sickness remedies in severe sea conditions". Wilderness Environ Med. 11 (2): 136–7. doi:10.1580/1080-6032(2000)011[0136:LTTE]2.3.CO;2. PMID 10921365.
  6. Shri Kamal Sharma (1 January 1992). Resource Utilization and Development: A Perspective Study of Madhya Pradesh, India. Northern Book Centre. pp. 1078–. ISBN 978-81-7211-032-1. Retrieved 30 June 2013.
  7. Norfleet, W. T.; Peterson, R. E.; Hamilton, R. W.; Olstad, C. S. (January 1992). "Susceptibility of divers in open water to motion sickness". Undersea Biomed Res. 19 (1): 41–7. PMID 1536062. Retrieved 2008-05-09.
  8. Lawson, B. D. (2014). Motion sickness symptomatology and origins. Handbook of Virtual Environments: Design, Implementation, and Applications, 531-599.
  9. So, R.H.Y. and Ujike, H. (2010) Visually induced motion sickness, visual stress and photosensitive epileptic seizures: what do they have in common? - Preface to the special issue. Applied Ergonomics, 41(4), pp.491-393.
  10. Wax, Emily (30 July 1999). "The Dizzy Spell of 'Blair Witch Project'". The Washington Post. Retrieved 8 February 2017.
  11. "Combating VR Sickness: Debunking Myths And Learning What Really Works". ARVI Games.
  12. "The National Advanced Driving Simulator - The NADS-1". Nads-sc.uiowa.edu. Retrieved 2014-03-02.
  13. So, R.H.Y.; Lo, W.T. (1999). Proceedings IEEE Virtual Reality (Cat. No. 99CB36316). pp. 237–241. doi:10.1109/VR.1999.756957. ISBN 978-0-7695-0093-5.
  14. CyberEdge Information Services: Health & Safety, Simulator Sickness in Virtual Environments: Executive Summary
  15. Kohl, R. L. (1983). "Sensory conflict theory of space motion sickness: An anatomical location for the neuroconflict". Aviation, Space, and Environmental Medicine. 54 (5): 464–5. PMID 6870740.
  16. Lackner, J. R. (2014). "Motion sickness: More than nausea and vomiting". Experimental Brain Research. 232 (8): 2493–2510. doi:10.1007/s00221-014-4008-8. PMC 4112051. PMID 24961738.
  17. Motion sickness: an evolutionary hypothesis
  18. Ebenholtz SM, Cohen MM, Linder BJ (November 1994). "The possible role of nystagmus in motion sickness: a hypothesis". Aviat Space Environ Med. 65 (11): 1032–5. PMID 7840743.
  19. Sherrington, C.S. (1893). "Further experimental note on the correlation of action of antagonistic muscles". Proceedings of the Royal Society. B53 (1693): 407–420. Bibcode:1893RSPS...53..407S. doi:10.1136/bmj.1.1693.1218. PMC 2403312. PMID 20754272.
  20. Milot JA, Jacob JL, Blanc VF, Hardy JF (December 1983). "The oculocardiac reflex in strabismus surgery". Can. J. Ophthalmol. 18 (7): 314–7. PMID 6671149.
  21. Kennedy, R.S.; Graybiel, A.; McDonough, R.C.; Beckwith, F.D. (1968). "Symptomatology under storm conditions in the North Atlantic in control subjects and in persons with bilateral labyrinthine defects". Acta Otolaryngology. 66 (1–6): 533–540. doi:10.3109/00016486809126317. hdl:2060/19650024320. PMID 5732654.
  22. Cheung BS, Howard IP, Money KE (June 1991). "Visually-induced sickness in normal and bilaterally labyrinthine-defective subjects". Aviat Space Environ Med. 62 (6): 527–31. PMID 1859339.
  23. Ebenholtz, S.M.Oculomotor Systems and Perception. Cambridge University Press, 2005,148-153
  24. Previc, F.H. (2018). "An intravestibular theory of motion sickness". Aerospace Medicine and Human Performance. 89 (2): 130–140. doi:10.3357/AMHP.4946.2018. ISSN 2375-6314. PMID 29463358.
  25. Krueger WW (January 2011). "Controlling motion sickness and spatial disorientation and enhancing vestibular rehabilitation with a user-worn see-through display". Laryngoscope. 121 Suppl 2: S17–35. doi:10.1002/lary.21373. PMC 4769875. PMID 21181963.
  26. "Air Force to examine AdviTech's motion-sickness product for combat pilots". San Antonio Business Journal. Nov 10, 2010. Retrieved 15 July 2014.
  27. "BCMC, LLC". Retrieved 15 July 2014.
  28. "Google Glass Treating Motion Sickness". YouTube.com. Retrieved 15 July 2014.
  29. "Stroboscopic Vision as a Treatment for Space Motion Sickness" (PDF).
  30. Spinks A, Wasiak J (2011). "Scopolamine (hyoscine) for preventing and treating motion sickness". The Cochrane Database of Systematic Reviews (6): CD002851. doi:10.1002/14651858.CD002851.pub4. PMID 21678338.
  31. Schwartz, Henry JC; Curley, Michael D (1986). "Transdermal Scopolamine in the Hyperbaric Environment". United States Navy Experimental Diving Unit Technical Report. Retrieved 2008-05-09.
  32. Lawson, B. D.; McGee, H. A.; Castaneda, M. A.; Golding, J. F.; Kass, S. J.; McGrath, C. M. (2009). Evaluation of Several Common Antimotion Sickness Medications and Recommendations Concerning Their Potential Usefulness During Special Operations. (No. NAMRL-09-15) (Report). Pensacola, Florida.: Naval aerospace medical research laboratory.
  33. Bitterman N, Eilender E, Melamed Y (May 1991). "Hyperbaric oxygen and scopolamine". Undersea Biomedical Research. 18 (3): 167–74. PMID 1853467. Retrieved 2008-05-09.
  34. Williams TH, Wilkinson AR, Davis FM, Frampton CM (March 1988). "Effects of transcutaneous scopolamine and depth on diver performance". Undersea Biomedical Research. 15 (2): 89–98. PMID 3363755. Retrieved 2008-05-09.
  35. Arieli R, Shupak A, Shachal B, Shenedrey A, Ertracht O, Rashkovan G (1999). "Effect of the anti-motion-sickness medication cinnarizine on central nervous system oxygen toxicity". Undersea and Hyperbaric Medicine. 26 (2): 105–9. PMID 10372430. Retrieved 2008-05-09.
  36. East Carolina University Department of Diving & Water Safety. "Seasickness: Information and Treatment" (PDF).
  37. Brainard A, Gresham C (2014). "Prevention and treatment of motion sickness". Am Fam Physician. 90 (1): 41–6. PMID 25077501.
  38. Hemmerich, Wanja A.; Shahal, Avner; Hecht, Heiko (2019). "Predictors of visually induced motion sickness in women". Displays. 58: 27–32. doi:10.1016/j.displa.2018.11.005. ISSN 0141-9382.
  39. Hromatka BS, Tung JY, Kiefer AK, Do CB, Hinds DA, Eriksson N (May 2015). "Genetic variants associated with motion sickness point to roles for inner ear development, neurological processes and glucose homeostasis". Hum. Mol. Genet. 24 (9): 2700–8. doi:10.1093/hmg/ddv028. PMC 4383869. PMID 25628336.
Classification
External resources
This article is issued from Wikipedia. The text is licensed under Creative Commons - Attribution - Sharealike. Additional terms may apply for the media files.