Motion sickness

Vehicle motions

Motion sickness occurs when riding in a wide range of vehicles and even on animals. The main factors that determine the degree to which a motion may be provocative are the frequency and magnitude of motion.[19][20][21]
Analyses of motions that provoke motion sickness, together with experiments involving motion simulation, reveal that sickness occurs most readily with motion frequencies around 0.2 Hz (cycles per second) and declines at frequencies above or below.
Modern large ocean liners, which operate at 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. This is referred to as visually induced motion sickness (VIMS) and is a separate diagnosis to motion sickness caused by physical motion.[1]
Nauseogenic visual experiences include virtual reality displays, computer or television monitors, cinematographic projections, or simulators.[1] 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'.
A significant number of patients with migraine syndrome may experience VIMS.[1] It has been suggested that the pathophysiological mechanisms involved may be similar to those responsible for migraine symptoms.[22][23][24][25]
The illusion of self-motion stimulated by an optokinetic drum can elicit the full range of motion sickness symptoms, including nausea.[26]

Behavioural context

The development of motion sickness and intensity of symptoms may be exacerbated by activities that cause conflicting inputs from visual and vestibular systems (visuo-vestibular conflict).
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.[10]
A coherent perception of motion relies on integration of allocentric and egocentric sensory cues. In this process the degree to which a sensory modality is relied on is crucial, especially in cases where different sensory information are in conflict. 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 which is not moving relative to the head. 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 stationary in the cabin, sees the external landscape appearing to tilt.[27]
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.[27][28]
Environmental context, including the sight and smell of vomit, diesel fumes, and other unpleasant chemical and animal smells, may also lower the threshold for the development of symptoms.[29]

All vertebrates can experience motion sickness when encountering unusual turbulence, and those capable of vomiting may do so if the motion is sufficiently provocative. The development of motion sickness depends upon the integrity of the vestibular apparatus, or at least some functioning component of it, and how the vestibular inputs are integrated with other sensory information, such as visual inputs.

The neurophysiological and neurochemical mechanisms responsible for the provocation of nausea and vomiting by certain conditions of motion are largely unknown. The major structures and functions involved in producing motion sickness include vestibular inputs from the semicircular canals, the otolith organs, and the ‘velocity storage’ integrator within the vestibular nuclei. These structures have extensive connections with the ocular motor and autonomic centres within the brainstem, cerebellum, and higher order centres within the cerebral hemispheres.[30][31] For motion sickness provoked specifically by combined head rotation and tilt, studies have found that adaptation to motion or suppressive effect of baclofen can reduce motion sickness through the velocity storage mechanism.[32][33][34] This mechanism 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. The bias produced by velocity storage is closely related to motion sickness and is independent of the magnitude of changes in head position.[35] Brain structures supporting velocity storage involve the vestibular nuclei and the uvula and nodulus of the vestibulo-cerebellum.[32][33] Other key inputs that can be involved in sensorimotor conflict that produce motion sickness include visual and proprioceptive inputs. Despite high intra-participant correlations between the magnitudes of eye movement 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.[36]

Low serotonin level was found as a candidate factor that may predispose normal individuals to motion sickness, highlighting similarities with migraine. Histamine intolerance has also been proposed as a predisposing factor.[37][38] However, it is less likely that a single neurochemical factor is responsible for susceptibility to motion sickness. Rather, involvement of multiple neurochemicals and their interactions is more likely to contribute to motion sickness.

Brain interpretation of movement

Vehicle motions that provoke motion sickness almost always challenge how people sense, perceive, or respond to orientation. 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 interpretation of the 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.[39][40][41][42] In this zone of ambiguity, the brain may become uncertain of how to interpret sensory input, and perceptual conflicts may arise between processing or integration of vestibular signals with other sensory cues. Thus, a key element in the nauseogenic process may be the development of an internal conflict in the processing of sensory inputs that contribute to spatial orientation.[43]
An important example of conflict is 'visuo-vestibular', typified by attempting to read in a car, which makes many people motion sick. The vestibular ocular reflexes, which move the eyes to maintain fixation on a stationary external environment, may conflict with visual fixation on the text, which is not moving relative to the head and does not necessitate eye movement.[10]
One possible explanation for the frequency separation between tilt and translation may lie in body mechanics. In some high-speed low-frequency activities, the head may tilt while the trunk and legs are thrust from side to side in high frequency. These distinct motions can be part of many activities such as running, cycling, or skiing.

There is unlikely to be a single explanation for the response of nausea or 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 twofold purpose of transducing head orientation and sensitivity to ingested toxins.[44][45]
Haemodynamic redistribution: vomiting relieves the stomach of digestive function so that blood can be directed to muscle activity to help 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 visuo-vestibular aberrant activation by unusual motion or neural mechanisms that normally maintain a stable internal environment.[3][46]

International classification of vestibular disorders (ICVD): motion sickness diagnostic criteria[1]

Motion sickness:

An acute episode of motion sickness is diagnosed when the sickness-inducing stimulus is physical motion of the person. This could be provoked by transportation (e.g., motion on a vehicle or animal), amusement devices (e.g., amusement park rides, playground equipment, hammocks), or swaying buildings.

Motion sickness disorder (MSD):

MSD is diagnosed when at least five episodes of motion sickness are reliably triggered by the same or similar motion stimuli, severity does not significantly decrease with repeated exposure, there is a behavioural or emotional response (such as avoiding or dreading the activity), and the symptoms are not better explained by another disorder.

Visually induced motion sickness (VIMS):

An acute episode of VIMS is diagnosed when the stimulus is visual motion. This could be provoked by virtual reality displays, computer or television monitors, cinematographic projections, or simulators.[4][5]

Visually induced motion sickness disorder (VIMSD):

VIMSD is diagnosed when at least five episodes of VIMS are reliably triggered by the same or similar visual stimuli, severity does not significantly decrease with repeated exposure, there is a behavioural or emotional response (such as avoiding or dreading the activity), and the symptoms are not better explained by another disorder.

Any combination of motion sickness, MSD, VIMS, and VIMSD can co-occur. The intensity of symptoms in response to physical or visual motion stimuli can vary greatly and may fluctuate in an individual due to factors like ageing, adaptation, or the presence of other medical conditions. For acute episodes of motion sickness or VIMS, symptom severity can be worsened by conditions like ocular motility disorders, visual-vestibular disorders, or vestibular disorders such as vestibular migraine, vestibular neuritis, or persistent postural perceptual dizziness. In such cases, both a diagnosis of motion sickness or VIMS and the underlying disorder should be made. See Criteria.

Pathophysiology

Classification

International classification of vestibular disorders (ICVD): motion sickness diagnostic criteria[1]