Motion sickness is a condition that happens in association with travel or movement when a difference occurs between visually perceived movement and the vestibular system’s sense of bodily movement. Most kinds are considered terrestrial motion sickness, such as being carsick, airsick, seasick, or sick from reality simulation.
Symptoms include dizziness, fatigue, vertigo, depressed appetite, nonspecific malaise, gastrointestinal discomfort, (most commonly) nausea, and nausea-caused vomiting. If the cause of the nausea is not resolved, the sufferer will usually vomit, but vomiting may not relieve the feeling of weakness and nausea, which means the person might continue to vomit until the underlying cause of the nausea is resolved.
“Nausea” in Greek means seasickness (naus means ship).
What Causes Motion Sickness?
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.
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. 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.)
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.
Defense Against Perception Of Poisoning
A very different alternate is the defense mechanism theory holding that motion sickness functions as a defense mechanism against neurotoxins. 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.
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.
Yet another theory, known as the nystagmus hypothesis, 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 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. 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; 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.
A recent theory 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).
Roughly one-third of the population is highly susceptible to motion sickness, and most of the rest may get motion sickness under extreme conditions. The incidence of space motion sickness has been estimated over the years at between forty and eighty percent of those who have entered 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, and that the risk decreases with advancing age.
There is some evidence that people with Asian ancestry may suffer motion sickness more frequently compared with 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.
Treatments For Motion Sickness
Many cures and preventatives for motion sickness have been proposed.. One common suggestion is to simply look out the window of the moving vehicle and to gaze towards the horizon in the direction of travel. This helps to re-orient the inner sense of balance by providing a visual reaffirmation of motion.
In the night, or in a ship without windows, it is helpful to simply close one’s eyes, or if possible, take a nap. This resolves the sensory conflict between the eyes and the inner ear. Napping also helps prevent psychogenic effects (i.e. the effect of sickness being magnified by thinking about it).
Fresh, cool air can also relieve motion sickness slightly, although it is likely this is related to avoiding foul odors which can worsen nausea.
Motion Sickness Devices
A motion blocking eyewear device was patented (US patent 6,275,998) to prevent carsickness-related terrestrial motion sickness. Visual cues are an important contributor to land-based vehicular travel in addition to vestibular (inner ear) input.
The eyewear device limits what the wearer sees outside the moving vehicle by use of an opaque shield. By removing visual cues outside the vehicle, the device normalizes the visual input dimension involved in sensory conflict, a leading theory behind motion sickness.
No evidence exists that motion blocking eyewear alters or eliminates vestibular input or that of other bodily receptors. Carsickness is the most common type of motion sickness given the number of travelers traveling over land versus those traveling by air or sea.
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. 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 (US Patent 5,966,680). This technology has been implemented in both standalone devices and Google Glass. In two NIH-backed studies, greater than 90% of patients experienced a reduction in the symptoms of motion sickness while using this technology.
Experiments with adaptation to reversion or inversion of the field of view showed the possibility of preliminary adaptation to the conflicts of the visual analyzer with other signals entering from vestibular system.
Over-the-counter and prescription medications are readily available, such as dimenhydrinate commonly known as dramamine, scopolamine, meclizine, promethazine, cyclizine, and cinnarizine. Several of these are antihistamines, with mild sedation being a common side effect. Cinnarizine is not available in the United States, as it is not approved by the FDA.
As these medications often have side effects, anyone involved in high-risk activities while at sea (such as SCUBA divers) must evaluate the risks versus the benefits. Promethazine is especially known to cause drowsiness, which is often counteracted by ephedrine in a combination known as “the Coast Guard cocktail”. There are special considerations to be aware of when the common anti-motion sickness medications are used in the military setting where performance must be maintained at a high level.
Scopolamine is effective and is sometimes used in the form of transdermal patches (1.5 mg) or as a newer tablet form (0.4 mg). The selection of a transdermal patch or scopolamine tablet is determined by a doctor after consideration of the patient’s age, weight, and length of treatment time required.
Ginger root is commonly thought to be an effective anti-emetic, but it is ineffective in treating motion sickness.
Thomas G. Dobie Motion Sickness: A Motion Adaptation Syndrome Springer; 1st ed. 2019 ISBN: 978-3319974927