Motion sickness: Aetiology, Pathophysiology & Epidemiology

Motion sickness is characterised by stomach discomfort, nausea, and vomiting, accompanied by autonomic features such as pallor and sweating. 

Vomiting often provides temporary or permanent relief of these symptoms. 
Once a certain level of nausea is attained, vomiting is almost inevitable, even if the patient is removed from the motion environment.

The rate at which motion sickness develops varies with the intensity of motion. 

Nausea leading to vomiting may develop within a few minutes if the provocative motion stimulus is intense, whereas with moderately provocative motion the onset of nausea is delayed, and vomiting may not necessarily occur. 

If motion is sustained, as on a long sea voyage, most people develop some habituation and become less susceptible to motion sickness. 

Similarly, frequent short exposures to provocative motion lead to a protective habituation, although the ability to adapt is marked by substantial individual differences. With infrequent exposures the protective value of habituating experiences is lost, and the patient returns to baseline levels of susceptibility. [Ref-1]

Aetiology (Causes)

Vehicle motions

  • Motion sickness occurs when riding in a wide range of vehicles and even on animals. The main factors determining how provocative a given motion may be are mechanical frequency tuning and magnitude of motion.[Ref-2]
  • Analyses of motions that provoke motion sickness, together with experiments involving motion simulation, reveal that sickness occurs most readily with mechanical motions circa 0.2 Hz (cycles per second) and declines with frequencies of motion above and below.
  • Modern large ocean liners, whose movements involve very low frequencies, are not particularly nauseogenic; similarly, riding in a ski boat or riding a horse, both of which involve high mechanical frequencies, may induce fear and discomfort but are not particularly nauseogenic.
  • In contrast, the mechanically smooth movements of a car, a tilting train (high-speed train with a tilting mechanism to increase speed on curved railway tracks [e.g., Acela Express from Washington, D.C. to Boston]), or a medium-sized boat, all of which involve frequencies of motion about 0.2 Hz, readily provoke motion sickness.
  • The frequency of motion sickness is also determined by the intensity of motion, so that even with a frequency much lower or higher than 0.2 Hz, sickness will occur if motion is sufficiently vigorous.
Environmental motions

  • Experiences of simulated visual motion can cause dizziness, nausea, and vomiting.
  • Nauseogenic visual experiences include virtual reality displays, cinemas, computer animations, and even television. 
  • In addition to inducing sensations of self-motion and nausea, modern computerised displays also induce disorientation with consequential loss of performance, a condition that has been termed 'cybersickness'.
  • The kinds of symptoms provoked by visual motion differ somewhat from those experienced with true self-motion. The most significant symptom provoked by visual flow is possibly headache, and it has been suggested that pathophysiological mechanisms similar to those responsible for migrainous phenomena may be involved. 
  • The illusion of motion stimulated by an optokinetic drum elicits the full range of motion sickness symptoms, including nausea.[Ref-3]
Behavioural context

  • The development of motion sickness and intensity of symptoms may be exacerbated by activities such as reading.
  • There are several factors involved. At a mechanical level, body and particularly head movements within a vehicle may simply increase the intensity of provocative motion stimuli. A particularly important factor is movement of the head within the framework of the vehicle, which is itself moving, such as a car turning a corner. These may provoke unusual and intense stimulation of the three-dimensional, semicircular canals and otolith organs of the labyrinth, which imparts intense dizziness and false perceptions of self-motion.
  • Physiological factors enhancing motion sickness usually involve a conflict between sensory inputs. The classic case is trying to read in a moving car: the vestibular ocular reflexes, which stabilise the eyes on external stationary objects, must be suppressed by visually guided eye movements in order to maintain scanning fixation on the text that is moving with the protagonist. A similar conflict arises in high-speed tilting trains (or an aeroplane making a coordinated turn when it comes in to land or takes off), which are particularly nauseogenic if the passenger, who feels completely upright in the cabin, sees the external landscape appearing to swing dramatically up and down.
  • Prominent among the numerous psychological factors that enhance motion sickness are anticipation of an unpleasant experience and the attempted execution of spatially loaded tasks such as map reading.
  • Environmental context, including the sight and smell of vomit, diesel fumes, and other unpleasant chemical and animal smells, also lowers the threshold for the development of symptoms.


All vertebrates, when encountering unusual turbulence, can become motion sick, and those able to vomit do so if motion is sufficiently provocative. The only caveat is that the development of motion sickness depends upon the integrity of the vestibular apparatus, or at least some functioning part.

The neurophysiological and neurochemical mechanisms responsible for the provocation of nausea and vomiting by certain conditions of motion are largely unknown. 

The major structures involved are the vestibular system and extensive connections with the cerebellum and with brainstem and higher mechanisms of autonomic function.

For motion sickness provoked specifically by combined rotation and tilt, several studies have found that adaptation to motion or suppression of motion sickness by baclofen reduces the 'velocity store' component of vestibular canal function. 

'Velocity store' is a neuronal process that extends vestibular signals of rotation during prolonged movement and helps to redirect eye movement during sequential, multi-axial head rotations. Brain structures supporting velocity store involve the vestibular nuclei and the uvula and nodulus of the vestibulo-cerebellum.

Despite high intra-participant correlations between eye movement magnitudes and susceptibility to motion in adaptation studies, inter-participant variability in eye movement responses to motion is too great for them to serve as a marker of baseline susceptibility to motion sickness. 

The onset of gastric dysrhythmias (e.g., tachygastrias) precedes the first report of nausea in healthy people during nausea induced by an optokinetic drum.

Low serotonin level is a candidate neurochemical factor that may predispose to motion sickness in normal individuals, highlighting similarities with migraine. Histamine intolerance has also been proposed as a predisposing factor.

Interpretation of movemen

  • Vehicle motions that provoke motion sickness almost always challenge how people sense, perceive, or respond to verticality. 
  • For prolonged accelerations of low-frequency content the body is preferentially perceived as tilted; for example, when taking off on an aircraft, one feels tilted backwards before the nose wheel actually lifts off the tarmac. 
  •  For rapid to-and-fro motion of high-frequency content such as rocking on a train, the preferential perception is of oscillatory translation. 
  • In parallel with perception, the vestibular-reflex eye movements evoked by low-frequency motion are a counter-rolling of the eyes, appropriate for tilting the head, whereas the response to high-frequency head movement is lateral eye movements, which compensate for the head movement to help fixate on stationary objects.
  • It is generally proposed that the decision to interpret movement as tilt or translation is served, in part, by frequency filtering vestibular signals so that low frequencies are interpreted to signify tilt. The frequency tuning of nauseogenic motion about 0.2 Hz spans the transition between preferential interpretations of motion as tilt or translation. 
  • In this zone of ambiguity the brain is uncertain of how to interpret sensory input, and perceptual conflicts may exist between vestibular processing and the behavioural context. Thus, a key element in the nauseogenic process is the development of an internal conflict in the processing of spatial orientation.
  • An important example of conflict is 'visual-vestibular', typified by attempting to read in a car, which makes many people motion sick. The vestibular ocular reflexes, which stabilise the eyes on the stationary external environment, are in conflict with visual fixation on the text, which is moving with the protagonist.
  • A possible explanation of the frequency separation of tilt-translation is that the constraints of body mechanics determine that the body must tilt for high-speed low-frequency manoeuvres, whereas the trunk and legs are thrust from side to side during high-frequency manoeuvres. These distinct tactics are apparently at work in many activities, such as running, cycling, or skiing. However, the transition from low- to high-frequency movements is a difficult tactic.

There is unlikely to be a single explanation for the response of vomiting, which could be attributable to a combination of proposed mechanisms including the following.

  • 'Toxin theory': the internal conflicting sensory or perceptual states resulting from certain kinds of motion are similar to the consequences of ingesting a neurotoxin, which the body expels by vomiting. As a corollary the vestibules have evolved for the 2-fold purpose of transducing head orientation and sensitivity to ingested toxins.
  • Haemodynamic redistribution: vomiting relieves the stomach of digestive function so that blood can be directed to muscle activity to help the protagonist resolve the motion challenge.
  • Anxiety: initial symptoms of nausea alert the person to the distressing situation, and as with other severe anxiety states, can lead to vomiting.
  • Chaotic autonomic response: motion sickness results from visual-vestibular aberrant activation by unusual motion or neural mechanisms that normally maintain a stable internal environment.


According to transport surveys, individual susceptibility to motion sickness appears to develop sometime during childhood, peak at around the age of puberty, and thereafter slightly decline through adulthood. Children aged 2-12 years are particularly susceptible to motion sickness, while older adults (aged >50 years) are less susceptible.

Actual vomiting appears to be infrequent beyond teenage years.

There are wide variations in susceptibility to motion sickness, but only those individuals with a non-functional vestibular system are truly immune. 

In highly provocative environments, such as on a life raft in rough seas, all people can become motion sick. 

Although the impact of motion sickness on activities of daily life has not been surveyed extensively, about one third of people experience significant symptoms when riding in vehicles; with passenger illness occurrence three times higher for passengers with no view of the road ahead compared to passengers who could see the road ahead extremely well.

In extreme cases of individuals with the highest levels of susceptibility, moderate motions may induce severe motion sickness that causes incapacitating malaise including nausea, dizziness, and headache, which may last throughout motion and for hours afterwards. Women are more susceptible to motion sickness than men; women show a higher incidence of vomiting and report a higher incidence of symptoms such as nausea. 

A 5:3 female-to-male risk ratio for vomiting has been shown for ferry passengers.

There is evidence that there is a slightly higher susceptibility among people of Chinese ancestry.
Motion sickness: Aetiology, Pathophysiology & Epidemiology
Dr.Tamer Mobarak


No comments
Post a Comment