REVIEW

URRENT
C
OPINION

Pathophysiology and treatment of motion sickness

John F. Golding a and Michael A. Gresty b

Purpose of review
Motion sickness remains bothersome in conventional transport and is an emerging hazard in visual
information technologies. Treatment remains unsatisfactory but advances in brain imaging,
neurophysiology, and neuropharmacology may provide insights into more effective drug and behavioural
management. We review these major developments.
Recent findings
Recent progress has been in identifying brain mechanisms and loci associated with motion sickness and
nausea per se. The techniques have included conventional neurophysiology, pathway mapping, and
functional MRI, implicating multiple brain regions including cortex, brainstem, and cerebellum.
Understanding of the environmental and behavioural conditions provocative of and protective against
motion sickness and how vestibular disease may sensitize to motion sickness has increased. The problem of
nauseogenic information technology has emerged as a target for research, motivated by its ubiquitous
applications. Increased understanding of the neurophysiology and brain regions associated with motion
sickness may provide for more effective medication in the future. However, the polysymptomatic nature of
motion sickness, high interindividual variability, and the extensive brain regions involved may preclude a
single, decisive treatment.
Summary
Motion sickness is an emerging hazard in information technologies. Adaptation remains the most effective
countermeasure together with established medications, notably scopolamine and antihistamines.
Neuropharmacological investigations may provide more effective medication in the foreseeable future.
Keywords
motion sickness, neurophysiology, vestibular, virtual reality

INTRODUCTION

dizziness, and, unsurprisingly, loss of appetite and

increased sensitivity to odors [1 ]. The importance
and negative impact on performance of sopite is
underestimated [2 ], and yawning has been shown
to be a behavioural marker [3 ]. The headache provoked can be migrainous and disabling [1 ]. Gastric
dysrhythmias may provide a marker of nausea in
motion sickness [4], and drop in stomach fundus
and sphincter pressure correlates with nausea [5 ].
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A resurgence of interest in motion sickness in recent

years has been attributable to the use of nauseogenic
visual displays and realization of the involvement of
the vestibular system, the key mechanism in motion
sickness, with clinical disorders including migraine.
Nonetheless, characteristic of the history of motion
sickness studies, progress has been slow. Some of the
central neuronal pathways involved in processing of
provocative stimuli have been identified. There is
greater understanding of the environmental and
behavioural circumstances and medical conditions
that modulate motion sickness, but little advance
in treatments.

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PROVOCATIVE CIRCUMSTANCES
In an extensive survey of a cruise ship, motion sickness was the most common reason for physicians
a

SYMPTOMATOLOGY
Motion sickness is polysymptomatic. Nausea and
vomiting may be accompanied by a host of significant symptoms including headache, sopite (drowsiness), sweating, facial pallor, cold sweating,
increased salivation, sensations of bodily warmth,

Department of Psychology, University of Westminster and bDivision of

Brain Sciences (Neuro-Otology Unit), Imperial College London, Charing
Cross Hospital, London, UK
Correspondence to Prof John F. Golding, Department of Psychology,
University of Westminster, 309 Regent Street, London W1B 2UW, UK.
Tel: +44 2079115000; e-mail: goldinj@westminster.ac.uk
Curr Opin Neurol 2015, 28:8388
DOI:10.1097/WCO.0000000000000163

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Neuro-ophthalmology and neuro-otology

interpretations and, thus, a frequency region of

maximal uncertainty concerning the appropriate
frame of reference for orientation. A related ecological explanation has been proposed that this
frequency tuning is related to mechanical limitations on human body motion. This proposes that a
cause of motion sickness may be the difficulty in
selecting appropriate tactics to maintain body
stability at vehicle motion circa 0.2 Hz, between
whole-body GIF alignment, seen at lower frequencies, versus lateropulsion, seen at higher frequencies
[1 ].

KEY POINTS
 Habituation remains the most effective treatment for
motion sickness.
 There have been very few practical advances in
antimotion sickness medication over the standard
treatments such as scopolamine or antihistamines.
 Visually induced motion sickness through new
technologies such as 3D displays has emerged as a
significant new source of motion sickness.

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 There has been significant progress in mapping

neurophysiological pathways associated with nausea
and motion sickness, which may provide a more
rational basis for future treatments.

MECHANISMS AND THEORIES

consultations, the incidence of 4.2 per 1000 person/

days being higher than for infections or injuries [6 ].
Up to a quarter of codrivers became motion sick in
rally cars if they were reading a book or sitting in the
back seat [7]. Although motion perception sensitivity
to off-vertical axis rotation increased immediately
after return from spaceflight compared to prespaceflight, motion sickness susceptibility decreased [8].
Vection can be induced using auditory cues,
although weaker than visually induced vection,
and unlike visual motion, auditory cues for motion
fail to produce sickness [9]. The addition of body
loads while standing can modulate both postural
sway and motion sickness induced by visual motion
[10]. Watching 3D stereoscopic video films provokes
more motion sickness than 2D videos [11 13 ]. By
contrast, another study in both adults and children
found only low levels of sickness, with no clear
differences between 2D versus 3D, and concluded
that use of a stereoscopic 3D system for up to 2 hours
was acceptable for most users regardless of age [14 ].
With vehicular movement, nauseogenicity peaks
at a mechanical frequency of around 0.2 Hz, and this
has also been shown true for exposure to oscillating
visual field motion [15 ]. Hypotheses for the frequency dependence of nauseogenicity include a phase
error in signalling motion between canalotolith and
somatosensory systems, or a frequency-dependent
phase error between the sensed vertical and the
subjective or expected vertical. It has also been
proposed that a zone of perceptuomotor ambiguity
around 0.2 Hz triggers sickness, because at higher
frequencies, imposed accelerations are usually
interpreted as translation of the self through space,
whereas at lower frequencies, imposed accelerations are usually interpreted as a tilt in the gravitoinertial force (GIF) vector [1 ]. The region of
0.2 Hz would be a crossover between these two
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The generally accepted explanation of the how of

motion sickness is based on some form of sensory
conflict or sensory mismatch between actual versus
expected invariant patterns of vestibular, visual, and
kinaesthetic inputs as predicted by an internal
model [1 ]. Oman and Cullen [16 ] have identified
brainstem and cerebellar neurons whose activity corresponds to what might be expected of putative
sensory conflict neurons. The pathways that integrate vestibular and emetic gastrointestinal signals
that produce nausea and vomiting are being elucidated [17 ]. Galvanic vestibular stimulation in the cat
produces patterns of neural activation revealed by cfos labelling, some of which correlate with overt signs
of motion sickness, others of which show no such
relationship but may relate to covert affective aspects
such as nausea [18 ]. The onset of visually induced
nausea in humans was studied with functional
MRI. Increased activity preceding nausea was found
in the amygdala, putamen, and dorsal pons/locus
coeruleus, whereas, with onset of nausea, activity
was observed in a broader network including insular,
anterior cingulate, orbitofrontal, somatosensory,
and prefrontal cortices. Strong nausea was associated with sustained anterior insula and midcingulate activation, suggesting a close linkage
between these specific regions and nausea perception
[19 ].
By contrast with the how of motion sickness,
(i.e., the mechanisms), there is a variety of opinion
concerning the why. The most popular theory is
that motion sickness could have evolved from a
system designed to protect from potential neurotoxin ingestion by inducing vomiting when unexpected central nervous system inputs are detected
that might indicate poisoning (the toxin detector
hypothesis) [1 ]. This evolutionarily ancient system
is inadvertently activated by motion that causes
mismatch. Alternative hypotheses propose that
motion sickness could be the result of aberrant
activation of vestibularcardiovascular reflexes; it
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Pathophysiology and treatment of motion sickness Golding and Gresty

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100

MS susceptibility 95% CI

may be an unfortunate consequence of the physical

proximity of the motion detector (vestibular) and
vomiting circuitry in the brainstem or originate
from a warning system that has evolved to discourage self-exposure to circumstances causing disorientation or motor instability [1 ]. Recent variants of
the last idea postulate that motion sickness evolved
to discourage risky activity in the ancestral fish that
were suffering vestibular malfunction [20] or protohominids would avoid looking for food in swaying
trees that might threaten security, thus tending to
survive [21].

Comparison bs control
*P < 0.05 **P < 0.01
***P < 0.001 (total n = 326)

80

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60

40

20
**
0
Control

MARKERS FOR INDIVIDUAL

SUSCEPTIBILITY
Monozygotic and dizygotic twin studies indicate
human heritability of motion sickness having a
concordance of 70% in childhood decreasing to
55% in adulthood, probably because of habituation
to differential environmental effects [1 ]. In shrews,
selective breeding for high versus low motion sickness susceptibility strains has shown the importance
of genetic determinants and that this extends to
anaesthesia-induced emesis, indicating some common mechanisms [22 ]. Very young children are
relatively immune to motion sickness, susceptibility
then increasing and peaking at around 9 years [23 ].
Susceptibility then progressively declines through
adolescence, adulthood, and old age although there
are great individual differences [24 ]. Females tend
to be more susceptible than males although this has
a smaller effect size than age. At around menopause,
female susceptibility appears to show a transient
increase versus their age-equivalent male contemporaries [24 ]. The reason for this is unknown but
there may be contribution from changes in migraine
headaches to more vertigo-like symptoms that
peak around menopause in women, an effect that
is not seen in men over the same age period (Thomas
Lempert, Berlin, Germany, personal communication). Personality traits such as higher anxiety
only show very small relationships with motion
sickness susceptibility [1 ,24 ].
Some special groups are at lower or higher risk
for motion sickness as revealed by studies using both
validated self-report motion sickness susceptibility
questionnaires and nauseogenic off-vertical axis
rotation [24 ,25 ] (Fig. 1). Compared with controls, patients with bilateral vestibular loss (BVL)
are either completely resistant to motion sickness
or have very low symptom scores. The observation
that some patients with BVL can still exhibit some
degree of motion sickness is reminiscent of early
reports that pseudocoriolis motion could elicit
motion sickness in some patients with BVL [1 ]
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BVL

UVL

Vestib BPPV Vestib Clinical

neuritis
migraine migraine

FIGURE 1. MS susceptibility scores are shown for patient

groups together with significances of comparison with ageequivalent healthy controls. The 95% CI is smaller for
controls as a consequence of larger numbers. MS
susceptibility for Menieres disease is not shown because of
small numbers but is probably similar to migraine groups.
BPPV, benign paroxysmal positional vertigo; BVL, bilateral
vestibular loss; CI, confidence interval; MS, motion sickness;
UVL, unilateral vestibular loss [24 ,25 ].
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perhaps indicating that other types of sensory conflict without vestibular input are sometimes
possible. Unilateral vestibular loss (UVL) also
decreases susceptibility but to a lesser extent than
BVL; however, it should be noted that these were
compensated patients with UVL, that is, who have
adapted to sensory conflict caused by the loss of
vestibular function on one side, since in the acute
phase, the usual observation is that patients with UVL
may be more sensitive to motion. Patients with vestibular neuritis and benign paroxysmal positional
vertigo show no overall difference in susceptibility
compared with controls but within this broad picture
many individuals have up or downregulated their
sensitivity to motion in response to their disease.
Vestibular migraine leads to greatly elevated
susceptibility and patients attending migraine clinics, but without vestibular migraine, have equivalent elevations of susceptibility. Other recent studies
have shown that vestibular symptoms including
motion sickness are greater in patients diagnosed
with migraine as opposed to tension-type headache
[26]. Some patients with vestibular disease may
show higher motion sickness susceptibility to optic
flow [27]. A telephone survey suggested that
patients with Menieres disease had elevated
motion sickness susceptibility compared with controls but not as elevated as patients with vestibular
migraine [28].

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Physiological markers for predicting motion

sickness susceptibility have proved elusive.
Although motion sickness produces profound autonomic changes, baseline autonomic characteristics
are unlikely to provide useful predictors [29]. The
evidence that individual differences in postural
stability or perceptual style are good predictors of
motion sickness susceptibility seems limited and
contradictory [1 ,15 ,30 ]. Shorter time constants
of the central vestibular velocity store have been
suggested to correlate with reduced motion sickness
susceptibility [30 ], but there is sufficient contrary
evidence to question if this is a reliable predictor; it
has been suggested that it is not the duration of the
time constant per se, but the ability to modify readily
the time constant that may be a candidate marker
for success in motion sickness habituation [1 ]. In a
similar vein, reduced thresholds for cervical vestibular-evoked myogenic potentials predict future
habituation to seasickness, the suggestion being
that cervical vestibular-evoked myogenic potentials
at lower thresholds indicates that the individual has
broader dynamic range in which the reflex can
respond and adapt to a wider array of stimulus amplitudes [31]. Individual differences in brain white matter structure revealed by functional MRI may relate to
nausea susceptibility [32]. Patients with persistent
Mal de debarquement syndrome exhibit impaired
postural stability but do not exhibit differences
in intracortical excitability compared with controls [33].
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motion-induced nausea [39]. Exertion of control

reduced motion sickness induced by playing video
games on a tablet computer [40]. Lying supine, or
aligning the body with changes in the GIF environment, or avoiding head movements can reduce
motion sickness [1 ]. Consistent with the latter
observation, passive restraint of head, shoulders,
hips, and knees reduced motion sickness induced
by playing a video game while standing [41].
It has long been known that view of a stable
horizon reference can increase resistance to motion
sickness [1 ] but provision of an artificial horizon
failed to have any effect on Mal de debarquement
[42]. Standing with a wider stance width and view of
the horizon may reduce postural instability and
motion sickness at sea [43 ]. Stroboscopic illumination protected against motion sickness for back
seat military helicopter personnel, perhaps by
reducing retinal slip [44 ].
Controlled regular breathing has been shown to
provide increased motion tolerance, and may
involve activation of the known inhibitory reflex
between respiration and vomiting [34]. Acupressure
bands or electroacupuncture have produced conflicting findings as to their effectiveness against
motion sickness [34]. Although galvanic vestibular
stimulation (GVS) can cause vertigo and nausea, the
opposite effect has been proposed that it may provide a novel, modulatory countermeasure for
motion sickness [45]. GVS synchronous with the
visual field may normalize electrogastrographic
and autonomic responses and reduce motion sickness during flight simulation [46 ]. Repetitive transcranial magnetic stimulation can reduce symptoms
for Mal de debarquement syndrome [47].
Providing pleasant (or unpleasant) scents had
no effect on motion sickness sensitivity, although
motion sickness does enhance sensitivity to odors
[48]. Listening to pleasant music can reduce visually
induced motion sickness [49]. Positive verbal
instructions and placebo can promote reductions
in motion sickness [50].
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BEHAVIOURAL TREATMENTS AND OTHER

COUNTERMEASURES
Habituation offers the surest counter measure to
motion sickness being free of side-effects and
superior to drug treatments but, by definition, is a
long-term approach [34]. Optokinetic training gave
improvements in reducing seasickness in 71% of
those treated versus 12% of controls [35 ]. Motion
sickness decreases with repeated exposures to a
high-G flight simulator [36]. More comprehensive
motion sickness desensitization programmes are
highly effective and long-term success rates of
85% have been achieved [37 ]. Visual-vestibulosomatosensory conflict induced by virtual reality
increases postural instability and motion sicknesslike symptoms. Subsequently, the contribution of
visual inputs is reduced and such sensory reweighting may reflect adaptation to reduce the impact of
such visually provocative environments [38].
Being in control, as driver or pilot rather than
being the passenger, affords some protection against
motion sickness [1 ]. Similarly, enhanced perceptions of control and predictability appear to reduce
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PHARMACOLOGICAL
COUNTERMEASURES
Drugs currently used against motion sickness were
identified over 40 years ago [1 ]. They may be divided
into the following categories: antimuscarinics (e.g.,
scopolamine), H1 antihistamines (e.g., dimenhydrinate), and sympathomimetics (e.g., amphetamine).
Combinations for example scopolamine and dexamphetamine are highly effective since both drugs
combine their different antimotion sickness properties and their respective side-effects of sedation
and stimulation cancel each other out. However,
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Pathophysiology and treatment of motion sickness Golding and Gresty

such combinations are less used because of the

abuse potential of amphetamine. The main practical advances have been in drug delivery, such as
the transdermal scopolamine patch to provide
extended protection but with slow onset, and the
ongoing development of rapid acting intranasal
scopolamine. Other classes of potent antiemetics
are not effective against motion sickness, including
D2 dopamine receptor antagonists and 5HT3
antagonists used for side-effects of chemotherapy.
This is probably because their sites of action may be
at vagal afferent receptors or the brainstem chemoreceptor trigger zone, whereas antimotion sickness
drugs act elsewhere [1 ].
Approaches to developing new antimotion sickness drugs include re-examination of old drugs such
as phenytoin, as well as the development of newer
agents such as neurokinin1 antagonists. Such drugs
include phenytoin, betahistine, chlorpheniramine,
cetirizine, fexofenadine, benzodiazepines and barbiturates, the antipsychotic droperidol, corticosteroids such as dexamethasone, tamoxifen, opioids
such as the m-opiate receptor agonist loperamide,
neurokinin NK1 receptor antagonists, vasopressin
V1a receptor antagonists, N-methyl-D-aspartate
antagonists, 3-hydroxypyridine derivatives, 5HT1a
receptor agonists such as the antimigraine triptan
rizatriptan, and selective muscarinic M3/M5 receptor
antagonists such as zamifenacin and darifenacin
[1 ]. So far, none of these drugs have any advantage
over those currently available for motion sickness.
The reasons vary and include lack of efficacy and
complex pharmacokinetics or, in those that are effective, unacceptable side-effects.
Research, however, continues on drug treatment. Dexamethasone alleviates motion sickness
in rats in part by enhancing the endocannabinoid
system [51]. Cannabidiolic acid prevents both
motion or toxin-induced vomiting in shrews and
nausea-induced behaviour in rats [52]. The relative
effects on semicircular canal and otolith functions
by various antimotion sickness drugs including
meclizine, dimenhydrinate combined with cinnarizine, and promethazine combined with D-amphetamine may provide insights into their mechanism
of action [53]. Ginger (active ingredient gingerol)
may have antiemetic effects for motion sickness but
conflicting reports indicate that such effects are
weak [54].

pharmacotherapeutic research has mainly targeted

nausea and vomiting, so far, with little advantage
over established antimotion sickness drugs. Future
development of drugs with highly selective affinities
to receptor subtypes relevant to motion sickness may
produce an antimotion sickness drug of high efficacy
with few side-effects. However, the polysymptomatic
nature of motion sickness with its high interindividual variability may preclude a single decisive treatment. In this respect motion sickness is similar to
migraine, with which motion sickness is frequently
compounded.

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Acknowledgements
None.
Financial support and sponsorship
None.
Conflicts of interest
There are no conflicts of interest.

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READING
Papers of particular interest, published within the annual period of review, have
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&
of special interest
&& of outstanding interest

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CONCLUSION
Main advances in recent years have been in identifying brain mechanisms and loci that are associated
with motion sickness and/or nausea. Similarly,
although motion sickness is polysymptomatic,

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Volume 28  Number 1  February 2015

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