The Science Behind Motion Sickness

“Hey, can you stop here for a while? I’m feeling carsick.”

Have you ever experienced carsickness? The feeling of nausea because you sit in a moving vehicle for a while. Carsick, seasick, airsick, or even nauseous from riding an amusement park ride is considered MOTION SICKNESS! Other symptoms of this condition include malaise, pallor, cold sweating, and even vomiting. In general, motion sickness is established when these symptoms are provoked by motion (Money, 1970).

Fun fact! Do you know that different species have different susceptibilities to motion sickness? For example, dogs, horses, cows, and monkeys are reported to be susceptible to motion sickness; but rabbits and guinea pigs are reported to be immune to this condition! (Money, 1970)

But, how does this condition occur? And why do we have this motion sickness response in the first place? Well, in this article, we are going to discuss the scientific aspect behind motion sickness!

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The Science Behind Motion Sickness

Up until now, there is no concrete evidence of the mechanism of motion sickness. The generally accepted explanation of why motion sickness occurs is the sensory conflict/mismatch theory. This theory states that there is a difference between the expected and the actual patterns of vestibular, visual, and kinesthetic inputs.

The Vestibular System

Before we dive deeper into motion sickness, let’s discuss a little bit about the vestibular system!

The vestibular system is located in the inner ear and consists of the two structures of the bony labyrinth of the inner ear, the vestibule and semicircular canals, and the structures of the membranous labyrinth contained.

Figure 1. The vestibular system in the inner ear (Hussain et al., 2017)

The vestibular system detects the position and movement of our head in space, such as acceleration, gravitational forces, and tilting of the head (Casale et al., 2022).

The Sensory Conflict/Mismatch Theory

Now that we know that the vestibular system can sense the position and movement of our head, how is it involved in motion sickness?

Stott (1986) suggested what is considered to be the most practical model of motion sickness. This model stated that there are a set of conditions that when broken, would result in motion sickness:

1. Visual-vestibular: the motion of the head in one direction (sensed by the vestibular system) must result in the motion of the external visual scene in the opposite direction (sensed by the visual system)

2. Canal-otolith: the rotation of the head (sensed by the canals), except in the horizontal plane, must be accompanied by an appropriate angular change in the direction of the gravity vector (sensed by the otolith).

3. Utricle-saccule: any sustained linear acceleration that is due to gravity, has an intensity of 1 g, and defines as “downward”.

Therefore, when these conditions are altered, for example when you are closing your eyes in a moving vehicle or when the function of the vestibular apparatus is damaged due to some health conditions, motion sickness may be induced.

How Motion Sickness Causes Nausea and Vomiting

Other than the vestibular and visual system, the brain and gastrointestinal tract also plays part in motion sickness, especially in inducing nausea and vomiting. The concept is that there is a certain part of the brainstem called the “vomiting center”, that is often triggered by motion or toxins, resulting in signals that lead to nausea and vomiting.

Why Do We Even Have This Response?

Now that we have discussed how motion sickness occurs, let’s move to another question: why do we have this response in the first place? Well, the answer relays on the function of the vestibular system! Several hypotheses that have been proposed can be classified into:

Poison detector

This hypothesis proposes that the brain thinks that the mismatch between the expected and the actual patterns of vestibular, visual, and kinesthetic information is a result of the central nervous system malfunction, which may be caused by the ingestion of neurotoxins. Therefore, the brain sends signals to initiate vomiting in order to remove the toxin from our body (Treisman, 1977).

Vestibular cardiovascular/autonomic reflex

This hypothesis suggests that motion sickness is caused by the inappropriate activation of the vestibular-cardiovascular reflex, which normally works together to maintain homeostasis (Yates et al., 1998).

Vocabulary Builder 👨‍🏭 Homeostasis: self-regulating processes done by organisms to maintain stability and to adjust to conditions that are best for survival.

Disorientation/motor warning

This hypothesis states that motion sickness is like a “punishment” system to discourage movement and situations that would cause disorientation and motor instability (Guedry et al., 1998).

Nonfunctional evolutionary maladaptation

The last theory states that motion sickness is just “bad luck”, an unfortunate consequence of the motion detected by the vestibular system, and the activation of the “vomiting center” in the brainstem (Oman, 2012).

All these explanations are mere hypotheses and none of them are concluded to be 100% correct. However, mounting evidence has to favor either the toxin detector hypothesis or the “bad luck” evolutionary maladaptation hypothesis (Golding, 2016).

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Now that you know the science behind motion sickness, don’t panic if you experience one! It’s a very common condition and usually resolves within hours to days. But, if it does not go away on its own, there are several ways to ease this condition, such as trying to relax, looking at a stale object, and breathing fresh air (Brennan, 2016). But hopefully, you can travel and enjoy amusement park rides without experiencing motion sickness in the first place!

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References

• Brennan, D. (2016, October 6). Why Do I Get Motion Sickness? WebMD. Retrieved September 25, 2022, from https://www.webmd.com/cold-and-flu/ear-infection/motion-sickness

• Casale, J., Browne, T., Murray, I., & Gupta, G. (2022). Physiology, Vestibular System. StatPearls [Internet]. https://www.ncbi.nlm.nih.gov/books/NBK532978/

• Golding, J. (2016). Motion sickness. Handbook of Clinical Neurology, 371–390. https://doi.org/10.1016/b978-0-444-63437-5.00027-3

• Hussain, B., Ali, M., Qasim, M., Masoud, M. S., & Khan, L. (2017). Hearing impairments, presbycusis and the possible therapeutic interventions. Biomedical Research and Therapy, 4(4), 1228. https://doi.org/10.15419/bmrat.v4i4.159

• Money, K. E. (1970). Motion sickness. Physiological Reviews, 50(1), 1–39. https://doi.org/10.1152/physrev.1970.50.1.1

• Oman, C. M. (2012). Are evolutionary hypotheses for motion sickness “just-so” stories?1. Journal of Vestibular Research, 22(2–3), 117–127. https://doi.org/10.3233/ves-2011-0432

• Stott, J. R. R. (1986). Mechanisms and Treatment of Motion Illness. Advances in Applied Neurological Sciences, 110–129. https://doi.org/10.1007/978-3-642-70479-6_9

• Treisman, M. (1977). Motion Sickness: An Evolutionary Hypothesis. Science, 197(4302), 493–495. https://doi.org/10.1126/science.301659

• Yates, B. J., Catanzaro, M. F., Miller, D. J., & McCall, A. A. (2014). Integration of vestibular and emetic gastrointestinal signals that produce nausea and vomiting: potential contributions to motion sickness. Experimental Brain Research, 232(8), 2455–2469. https://doi.org/10.1007/s00221-014-3937-6

• Guedry FE, Rupert AR, Reschke MF (1998). Motion sickness and development of synergy within the spatial orientation system. A hypothetical unifying concept. Brain Res Bull, 47, 475-480.