Motion sickness is the nausea, disorientation and fatigue that can be induced by head motion. The first sign is usually pallor (a pale appearance). Yawning, restlessness and a cold sweat forming on the upper lip or forehead often follow. As symptoms build, an upset stomach, fatigue or drowsiness may occur. The final stages are characterized by nausea and vomiting.
Motion sickness is a general term. It can be subdivided into sickness due to visual stimulation, due to vestibular stimulation, and occasionally, forms occur associated with somatosensory stimulation (e.g. treadmill sickness), or head-on-neck motion (e.g. cervical vertigo). By far the most common subgroup are pure visual sensitivity -- usually called "visual dependence". In visual dependence, people become sick due to visual motion (such as going to a movie).
Motion sickness has been around as long as there has been people and motion. It was well known to the Greeks and Romans (Huppert et al, 2016). Around 300 AD the Chinese described "Cart-influence" and "Ship-influence" (Brandt et al, 2016). Admiral Nelson, the British naval hero who first went to sea at the age of 12, was a chronic sufferer.
Motion sickness is common and normal. Nearly anyone can be made motion sick by an appropriate stimulus, except for individuals with no vestibular system (William James). According to Benson, nearly 100% of (human) occupants of life rafts will vomit in rough seas. 60% of student aircrew members suffer from air sickness at some time during their training. For vertical motion (heave), oscillation at a frequency of about 0.2 hz is the most provocative. Motion at 1 Hz is less than 1/10th as provocative. About 7% of seagoing passengers report vomiting during a journey (Lawther and Griffin, 1988).
In a large study done in India, the prevalence of motion sickness was about 28%, and females were more susceptible (27%) were more susceptible than males (16.8%). Similarly, in Germany, the prevalence of answering "yes" to a question about motion sickness is about 13.4% overall, including 50% prevalence in persons < 30 years old. However prevalence is obviously dependent on how you define motion-sickness as nearly anyone can be made sick by motion, if it is vigorous enough. Individuals with more active occupations are less susceptible (Sharma, 1997). Interestingly, in medical transport personnel, 46% of personnel reported nausea and 65%, the Sopite syndrome (sleepiness caused by motion). (Wright, 1995)
Horses, cows, monkeys, chimpanzees, birds and sheep have been reported in scientific publications to show motion sickness. Rats, unfortunately I suppose, do not vomit so cannot serve as experimental subjects.
Women are more sensitive to motion than men, by a ratio of about 5:3, although this may be related to reporting differences rather than true physiological differences( Cheung, B. and K. Hofer , 2002). Women are more sensitive to motion around the times of their menstrual cycle (Glunfeld and Gresty, 1996). This may be due to interactions between migraine and motion sickness.
Children are said to be almost immune to motion sickness up to the age of 2. As children grow older, the severity of motion sickness increases up to roughly the age of 15 (Takahasi et al, 1994). In our dizziness practice, we have noticed women of childbearing age become more prone to motion sickness as their migraine tendency increases. There are two spikes of migraine in women of childbearing age -- one at 35, and another around menopause.
Recently, a genetic study of motion sickness was published in an "open access" type journal (Hromatka, 2015). They looked at 80,494 samples from a commercial personal genetics company, 23andme. They reported that there are 35 loci in their human genome sample, largely European ancestry, were associated with a greater propensity to develop motion sickness. Many of these locations were near genes involved in balance, eye, ear, and brain development. There was also an association between migraine, post operative nausea and vomiting (PONV), vertigo, and motion sickness. Both migraine and PONV shared genetic associations with motion sickness. One might think that a "fishing expedition" study like this, lacking any a-priori assumptions, could produce results due to chance alone. We hope that other similar studies emerge that can be compared with this one.
There are certain illness that eliminate motion sickness. These include bilateral loss of inner ear function (according to William James, the American Pragmatist philospher), and lesions of the cerebellar nodulus (Bard). As these illnesses are even worse than motion sickness, and there has been no attempt to use this observation clinically.
What Causes Motion Sickness ?
Although the dominant theory concerning motion sickness involves sensory conflict, there are also 2 other theories that "emphasize one of these responses, but deny the importance of the others" (Flanagan et al, 2004). As each of these situations occurs in nearly all motion, the question then becomes, which one is the most important.
Sensory conflict theory:
The sensory conflict theory is the dominant theory of motion sickness because it does the best job of explaining many types of motion sickness. There is a large literature about sensory conflict theory, as compared to a small number of papers supporting other theories. Sensory conflict theory is the favorite of the aerospace community (Oman, 1990).
In order for the body to determine where it is at all times, the brain combines visual information, touch information, inner ear information, and internal expectations. Under most circumstances, the senses and expectations agree. When they disagree, there is conflict, and motion sickness can occur.
For example, consider the situation when one is reading in the back seat of a car. Your eyes, fixed on the page, say that you are still. However, as the car goes over bumps and accelerates/decelerates, your ears disagree. This is why motion sickness in this situation is common. The driver has an advantage, as they have a better internal model of motion, and as well, their eyes are generally fixed on the outside world.
Another situation where motion sickness is common is in outer space. There, the otoliths no longer register the effect of gravity (which is no longer there), but continue to signal linear acceleration. It is presently thought that the very common space motion sickness is due to a loss of the usual otolith signal associated with head movement away from the gravitational axis. When the head is pitched, the brain misses the otolithic signal saying that pitch has occured, but continues to receive the canal signal. There is also another problem in outerspace in that linear acceleration may displace the inertial mass of an otolithic sensor, but rather than having gravity to restore it to resting position, only elasticity remains.
With respect to internal expectations, internal model theory suggests (rather reasonably), that much of brain processing can be viewed from the framework of considering that the brain builds an internal model of motion, to which it compares sensory input, and acts on the difference. Internal models then provide yet another source of conflict. One might expect then that motion sickness might be correlated with the veracity of the internal model. Somewhat supporting this idea, Guo et al (2017) reported that optokinetic afternystagmus time constant correlates with motion sickness susceptibility.
A partial vestibular loss (for a subset of otolithic input) is supposedly associated with strong motion sickness. Evidence that supports the conjecture that there is a long lasting "utricular syndrome" exists but is scanty. This conjecture is used to support extensive evaluations and habituation treatment procedures in motion sick individuals (e.g. https://www.dizziland.com). Looking at it from the opposite side, It is common to encounter asymmetrical oVEMP tests, in individuals who have no motion sickness. Singh et al (2014) reported that 1/3 of motion sick individuals have asymmetry of oVEMP or cVEMP, implying an asymmetry in utricular or saccular function across the ears. Scherer and colleagues proposed that asymmetrical otoliths were responsible for space motion sickness (Scherer et al, 1997). Vestibular testing involving centrifugation and shift of the subjective visual vertical is another method of looking for asymmetries. From a statistical perspective, this is a "fishing expedition" -- if one allows that asymmetry is either oVEMP OR cVEMP OR centrifugation asymmetry, thats quite a few lines in the pond ! Sensitivity is increased but specificity is decreased. In our opinion, the utricular syndrome is a possible mechanism for a subset of motion sick patients. As the saying goes, lack of evidence is not the same as evidence of lack, so it is a good idea to keep one's eyes open.
Reflexive eye movement theory
The essence of this theory is that it is just eye movement produced by retinal slip (i.e. relative movement of the world with respect to retina), that provokes motion sickness. Another way to put this, is that a reaction to a percieved high speed, produces motion sickness. There probably is a little bit to this theory, in that more motion likely causes more sickness, but we think the sensory conflict theory is much more reasonable. To put this in another way, we don't think that keeping the eyes fixed on a target that is moving with the person will prevent motion sickness.
Postural instability theory
This theory suggests that body movement, rather than eye movement or sensory conflict is the dominant influence on motion sickness. This theory has been advocated by Stoffregen et al (2013), and to our knowledge was first brought up by Fukuda in the 1970's. While postural instability often accompanies motion sickness, and there is probably some interconnection as well, we are dubious that this theory explains more than the sensory conflict theory. When there are interlocked phenomena it is sometimes difficult to separate chicken from egg. This looks more like an egg to us.
Acquired susceptibility to motion sickness is rare.
Migraine is a definite risk factor for motion sickness, with roughly a 5 fold greater incidence than non-migraineurs, and a roughly 50% prevalence (Marcus et al, 2005). See table below. Female gender and youth is also a risk factor. In women, days 9-15 of the menstrual cycle appear to have a higher incidence of nausea (Grunfeld and Gresty, 1999; Ramsay, 1994) but not all agree (Cheung, B., R. Heskin, et al. 2001). Medications that prevent migraine may also prevent motion sickness (see below).
|Table: Patients with Migraine having Motion Sickness|
|Percent of migraine patients with motion sickness||Comment||Authors|
|45%||Children (60)||Barabas et al (1983)|
|50.7%||Unselected||Kayan and Hood (1984)|
|50%||Marcus et al, 2005|
The space-military industrial complex has developed a theory of motion sickness that depends on asymmetry in otoconial mass (Scherer et al, 1997). Perhaps this mechanism is applicable in outer space, but it seems to us to have very little relevance to "down to earth". The more logical military explanation is the previously mentioned mechanism where the otoliths no longer provide gravity information.
Motion sickness is sometimes associated with prolonged vestibular responses (Hoffer et al. 2003), implying that these individuals simply appreciate motion more than others. On the other hand, motion sickness immunity is generally found in persons with absent vestibular responses (William James; Cheung et al. 1991). There is also less motion sickness in patients with vestibular loss (Paillard et al, 2013).
Age is probably not a large factor in motion sickness (Cheung and Money, 1992) although children below the age of 2 are said to be immune. They happily vomit. In our medical practice, the only substantial age effect seems to be in women who are experiencing migraines.
One way of testing for motion sickness is to ask people to fill out a questionnaire. There are many of these. Somewhat of an industry standard is the "MSSQ", or motion sickness susceptibility questionaire originally developed by Reason and Brand, and later shortened by Golding (1998, 2006) to become the "MSSQ-S" (for short). The "simulator sickness questionare" can be used to quantify how dizzy people get after motion. (Kennedy et al, 1992).
Another way to test for motion sickness is to move the subject being investigated about in a stimulating way and find out how long it takes for them to become sick. Certain activities, such as moving the head up and down while rotating, or "pitch while rotating", are very stimulating, and one can use the latency to vomit as a measure of motion sickness susceptibilty. As an example, Calkins et al (1987) reported on the "Coriolis sickness sensitivity index", the "staircase velocity movement test", and the "parabolic flight static chair test".
A third, very indirect, way is to determine how strong vestibular responses are, and to make the inference that people with no sensation will have no motion sickness. This idea probably originally derived from the observations of the pragmatist philosopher, William James, who was also interested in deafness, that persons without a vestibular system generally do not become motion sick. For example, Fowler et al (2014) reported that VEMPs were higher in young adults with motion sickness. Dai et al (2003) reported that aVOR time constants are inversely related to motion sickness. We have just not noticed this ourselves in our dizzy population.
Funtional MRI (fMRI) can show increased blood flow in parts of the brain in persons with induced motion sickness (e.g. Carvalho et al, 2021). This appears to us to be a "chicken/egg" problem, with a correlation being shown rather than a cause.
By way of a summary, we don't think that in general the method of assaying for motion sickness is a sensitive method of assaying for motion sickness susceptibilty. We think that practically, it is best to use some sort of standardized motion input and some sort of standardized output that correlates with nausea -- method 2.
There are three strategies to treat motion sickness:
- Behavioral (avoidance, mental activities)
- Medication (conventional, alternative)
- Exercise (habituation)
When all three strategies are used, it is extremely uncommon to find a person who does not get substantially better.
There are also some unproven procedures that we will discuss under the "experimental" heading.
Behavioral Strategies for Motion Sickness
One can often avoid motion sickness by anticipating the motion (Kuiper et al, 2019). Drivers have much less motion sickness than passengers, because they are controlling the motion, and know when they are turning, starting and stopping. Drivers on familiar routes are less prone to getting motion sick than drivers in new territory.
Medication for Motion Sickness
From a systems perspective, medication might change vestibular input (ordinarily always reduce), or reduce the consequences of motion stimulation. In other words, they might suppress input, or suppress central reactions to the input.
Most medications for motion sickness need to be taken at least 30 minutes before exposure to the activity that can cause the problem. Persons with glaucoma or prostate problems should not take most of these medications unless so advised by their doctor.
We so far have rarely encountered an individual who could not avoid motion sickness by pretreating with klonopin and ondansetron. That being said, here are more details.
Medications for nausea and vomiting
Treatment of motion sickness differs from treatment of nausea and vomiting. A discussion of the treatment of vomiting can be found here.
It is reasonable to assume that habituation (repeated motion exposure) makes one less motion sensitive. (Cheung, B. and K. Hofer, 2005). In fact, the military uses a "habituation" protocol to overcome motion sickness. This requires expensive equipment (a rotating chair). Habituation should be "batched" -- meaning done every day. There are a number of drugs which probably reduce habituation.
A somewhat similar approach was reported by Dai et al recently (2011), in a civilian apparatus. It again involved a rotatory chair as well as a simultaneously rotating optokinetic surround. In our practice in Chicago, we have abandoned the effort implement this protocol with our own equipment, but we have set up a similar protocol, also copied from work of Dai, using an optokinetic stimulus and the pseudocoriolis effect.
Habituation can be obtained through sports activities or physical therapy procedures. These procedures generally involve use of visual-vestibular mismatches, called "times 2" and "times 0" viewing. Stimulators with "disco balls" are often used too. We are unsure if these procedures are effective.
A home exercise method has been proposed to overcome motion sickness -- the "Puma" method. These exercises were developed by a flight surgeon (Sam Puma), to assist pilots with motion sickness in overcoming their sensitivity to motion. They are very stimulating exercises, that may be useful to extremely motivated people, who are not able to use more conventional methods of management of motion sickness such as medications. The Puma method appears to us to be a habituation protocol -- repeated exposure to the things that make one ill. This may well work -- if you can tolerate the process. We are cautiously hopeful about this method -- although it seems to us to be likely to cause a lot of nausea itself. When we sometimes suggest this to our patients in our dizziness practice, we suggest that they use ondasetron to avoid nausea. It is rare that someone with motion sensitivity is able to tolerate these exercises.
Activities that promote formation of "internal models" of motion may also be useful for motion sickness prevention. We do not know of any formal protocols that use this idea.
We recently have proposed a protocol for visual dependence that may be useful in treatment of motion sickness (Chang and Hain, 2007). See the page on visual dependence for more detail.