It has been stated that motion sickness is a normal reaction to an abnormal environment. In essence motion sickness is caused by exposure to complex, passive, and most often three-dimensional movements of the body in different environments such as cars, buses, trains, ships, airplanes, funfair rides or space travel. It is noteworthy that even mere visual immersion into a virtual reality environment without any body movement may cause motion sickness symptoms, though full blown sickness is rarely seen in such settings.

The most nauseogenic movements are  6]:

  • heave (up-and-down, elevator-like) motions,
  • rolling around the longitudinal axis,
  • yawing around the transversal axis,
  • and pitching around the transversal axis,


Apparently these different motion components may potentiate each other´s nauseogenic impact significantly, a condition which is the rule rather than the exception when at sea. In consequence, combined effects may lead to a stimulus well above the individual threshold for motion sickness.

The complex accelerations and decelerations as well as changes in the gravitational axis associated with these motions are perceived by movement, gravitation and equilibrium sensors (esp. otoliths in the labyrinth) and by proprioreceptors in muscles and tendons. However, they often cannot be matched with appropriate visual information. This is the case for instance in a ship cabin, where the passenger´s body feels the ship´s movements, however the cabin walls will remain static to the subject´s visual senses. But even if the passenger has a window to look out of, the reason for the acute movements will not be obvious in most instances, in particular on large ships.

This situation is addressed by the leading etiological hypothesis of motion sickness, called the „sensory mismatch theory“, alluding to conflicting sensory input as the major trigger of motion sickness. Visual system and vestibular system are predominant providers of postural information, however their relative importance may vary inter-individually. In subjects with impaired vestibular function the visual system may partially take over maintenance of postural control [7].

 In contrast, the modified „subjective vertical conflict theory“ postulates the importance of the >true< (gravitational) vertical axis for individual posture and balance. According to this hypothesis motion sickness is triggered by divergence between the plumb-line expected on the basis of formerly experienced patterns and the actual „real“ plumb line generated by sensory afferent impulses [8]. No matter which of those hypotheses comes closest to truth, a functioning vestibular system is an essential prerequisite for inducing motion sickness [5].

 Further to the above pathogenesis, afferent information in particular on posture and movements is sent to the brain stem from sources including the visual system, vestibular system, muscular proprioceptors, cochlea, cortex, limbic system, olfactory system and the intestine (esp. stomach via N. vagus). The sensory mismatch perceived by the brain triggers seemingly dysfunctional vegetative actions (vestibulosympathetic reflex), typically associated with motion sickness. This causes a stimulation of the emesis center located in the formatio reticularis, thus preparing to coordinate a potential subsequent act of vomiting.


Fig. 1 Central processing of afferences by the formatio reticularis (emesis center) in the brainstem. Nauseogenic information from the labyrinth (histaminergic afferences on posture, acceleration), the stomach (Nervus vagus, serotoninergic afferences), the limbic system (triggered by e.g. fear, disgust), and the chemo-triggerzone (dopamine- and opioid-receptors) are being received, weighed and in case of sufficient stimulus, retching and vomiting is initiated and coordinated. D2= Dopamine; H1= Histamine; M= Acetylcholine; 5-HT3= Serotonine (adapted from: Heintze K. Pharmaka mit Wirkung auf den Gastrointestinaltrakt. In: Estler CJ (Ed.). Pharmakologie und Toxikologie. 5. Aufl. Stuttgart, New York: Schattauer 2000). 


In motion sickness alterations in gastric wave patterns may be detected via electrogastrograms (EGGs), typically found shifted towards tachygastria (3.6-9.9 cpm), or mixed tachy- and bradygastria (1.0-2.4 cpm) [9;10;11]. In essence this >gastric arrhythmia< precludes a normal, coordinated propulsion of stomach content towards the duodenum and the distal GI tract, thereby increasing stomach distension and contributing significantly to nausea and vomiting.

 Cardiovascular reactions comprise a short-lived increase in blood-pressure (up to 10 mmHg), probably mediated via epinephrine, and tachycardia. An increase in peripheral blood flow (forearm) seems to be inversely correlated with resilience towards motions sickness [12]. Further down the line blood pressure usually decreases to hypotonic levels [13], which may be more pronounced by emesis-related fluid loss. An enhanced vasopressin (ADH) secretion in the motion sick has been observed by multiple investigators [11;15]. Its relevance is supported by the observation of tachygastria and nausea being induced by experimental vasopressin administration [16]. Individuals with increased resilience towards motion sickness stimuli also seem to generate lower vasopressin levels [[xii]]. One may speculate on the physiological function of vasopressin increase as a potential means to counterbalance the anticipated or imminent loss of fluid and electrolytes (via emesis), aiming at maintaining blood pressure via reduced diuresis.

Further observations of endocrine changes include increases in ACTH and ß-endorphines [17].

 Some factors contributing to individual predisposition to seasickness have been identified. People of Asian descent have a markedly reduced threshold (by –50% -65%) for experiencing symptoms of seasickness. This is in line with motion sickness tests demonstrating that Asian volunteers experience a higher intensity of nausea, and higher vasopressin levels compared to Caucasians, suggesting a genetic susceptibility to motion sickness and nausea [11;18]. Thus seafaring Asian nations such as ancient China have sought remedies for this „curse of navigation“, coming up with some usable approaches such as ginger root ingestion and acupressure.

Female gender also seems to enhance motion sickness susceptibility, and some fluctuation of susceptibility has been observed with the menstrual cycle [19]. Migraine may also increase sensitivity to motion stimuli and recent findings indicate that depletion of tryptophane, the serotonine precursor found in food such as egg, fish or cheese, may aggravate motion sickness susceptibility both in migraineurs as well as in healthy controls. This suggests that serotonine depletion may be an important factor in migraine and may as well facilitating motion sickness [19;20].

Schoolchildren experience an increased sensitivity to motion sickness that peaks around the age of 11 years for girls and as late as 21 years for male adolescents [21]. Patterns of postural stability acquired and refined throughout childhood and adolescence may not match with the afferent postural and labyrinthic impulses when at sea [22]. Conversely newborns and toddlers are resistant to motion sickness, fits well with their being passively carried around by their parents [23]. Ageing plays a positive role as motion sickness susceptibility usually decreases with age and gender differences eventually levelling [21].

 Golding et al. have devised a motion sickness susceptibility questionnaire (MSSQ-Short), which may serve to assess an individual´s proneness to become motion sick in reference to average benchmarks and percentiles. Past (childhood) motion sickness experience has a strong impact on the overall score. Apart from research purposes this questionnaire can be useful when assessing crew or advising travellers on prophylactic measures before boarding a cruise ship [24]: )


The MSSQ has also been found the best predictor for test-induced motion sickness, even exceeding ethnic and gender-related influences [18].


Further variables may often have decisive impact on induction and intensity of motion sickness:

  • Psychological factors such as an increased level of anxiety [25], situation related anxiety (i.e. fear of flying, fear of the Sea), mistrust or sensations of helplessness
  • Unpleasant smells (i.e. vomit, toilet, diesel fuel)
  • Time of day (increased sensitivity at night due to tiredness and the lack of compensational optical afferent data, in particular the horizon)
  • Tiring and exhaustion are rather strong co-factors that may significantly reduce the threshold for motion sickness
  • Lack of habituation (“getting one´s sea legs”) before strong stimuli occur (e.g. gale, high seas or swell), particularly during the start phase of a cruise
  • Alcohol may persist in the vestibular endolymphatic fluid for more than 24 hours and moderate to heavy alcohol intake may even lead to a loss of already acquired habituation

It remains enigmatic as to why motion stimuli may actually make people sick and helpless, instead of causing swift habituation or - at the other extreme - a „fight or flight“ adrenergic emergency reaction. Despite the high level of research conducted, the riddle of a potential physiology or utility behind motion sickness remains to be solved. Maybe this truly unpleasant syndrome is good for some purpose? One recent hypothesis postulates that the sensory mismatch as experienced in motion sickness may actually mimic an acute ingestion of toxins. This sounds convincing because intoxication and motion sickness are sharing symptoms such as nausea, vertigo and retching. Intoxication has been a serious threat throughout evolution of mankind, and triggering elimination of potentially lethal toxins via reduction of gastric propulsion and emesis may be considered a life-saving reflex [26]. This theory would also match with the age maximum observed in adolescents, being known for taking high risks and at the same time being comparatively inexperienced.