Physiological basis and pharmacology of motion sickness: an update

  title={Physiological basis and pharmacology of motion sickness: an update},
  author={Bill J. Yates and A. D. Miller and James B. Lucot},
  journal={Brain Research Bulletin},

The neural basis of motion sickness.

The source of the conflicts that cause the body to generate the autonomic signs and symptoms that constitute motion sickness are reviewed and a summary of the experimental data that have led to an understanding of how motion sickness is generated and can be controlled are provided.

Integration of vestibular and emetic gastrointestinal signals that produce nausea and vomiting: potential contributions to motion sickness

Additional neurophysiologic studies, particularly those conducted in conscious animals, will be crucial to discern the integrative processes in the brain stem that result in emesis, as much is left to be learned.

Brainstem processing of vestibular sensory exafference: implications for motion sickness etiology

It is proposed that conditions producing persistent activity of vestibular “sensory conflict” neurons, or their targets, stimulate nearby brainstem emetic centers—via an as yet unidentified mechanism.

Neural substrate for motion sickness: Involvement of the limbic system

Involvement of the amygdala may explain some characteristic features of motion sickness, such as its diversity of signs ranging from sympathetic to parasympathetic, and its conditioned occurrence where by some susceptible persons become sick even in motionless vehicles.

Motion sickness: more than nausea and vomiting

Substantial progress is being made in identifying the physiological mechanisms underlying the evocation of nausea, vomiting, and anxiety, and a comprehensive understanding of motion sickness may soon be attainable.

The Neurophysiology and Treatment of Motion Sickness.

The various types of motion sickness can be treated with general measures to lessen the intersensory conflict, behavioral changes, and drugs.

Processing of vestibular inputs by the medullary lateral tegmental field of conscious cats: implications for generation of motion sickness

Findings show that higher centers of the brain that are removed during decerebration regulate the labyrinthine inputs relayed to the LTF, either by gating connections in the brainstem or by conveying vestibular inputs directly to the region.

Motion sickness: A negative reinforcement model

  • B. Bowins
  • Psychology, Biology
    Brain Research Bulletin
  • 2010

The Physiology of Vomiting

Although vomiting is useful to avoid food poisoning, it is maladaptive in numerous clinical conditions, including treatments with cytotoxic cancer chemotherapy agents, inhalational anesthesia for surgery, and opioids for pain control; vomiting is also prominent in chronic diseases, such as diabetic gastroparesis and cyclic vomiting syndrome.



Motion sickness: a synthesis and evaluation of the sensory conflict theory.

  • C. Oman
  • Psychology
    Canadian journal of physiology and pharmacology
  • 1990
This paper reviews the types of stimuli that cause sickness and synthesizes a mathematical statement of the sensory conflict hypothesis based on observer theory from control engineering that describes the dynamic coupling between the putative conflict signals and nausea magnitude estimates.

Habituation and Motion Sickness

The rate of habituation when motion sickness was prevented by scopolamine was slowed, indicating that, if the central nervous system is not challenged by disruption of normal activation, it does not produce the compensatory reactions that result in habituation.

Organization of vestibular inputs to nucleus tractus solitarius and adjacent structures in cat brain stem.

In electrophysiological experiments, electrical stimulation of the vestibular nerve modified the firing rates of neurons located in the same regions of the NTS, suggesting that vestibulorespiratory reflexes are mediated by cells located elsewhere.

Integration of somatic and visceral inputs by the brainstem Functional considerations

A simple division of the brainstem into “somatic” and “autonomic” regions is no longer possible because movement and changes in cardiorespiratory activity often are coordinated, indicating a linkage between the pathways that control somatic motor activity and those that regulate respiration or circulation.

Sensory conflict theory and space sickness: our changing perspective.

  • C. Oman
  • Medicine
    Journal of vestibular research : equilibrium & orientation
  • 1998
The authors experience vigorous vestibular stimulation when they run, jump, or dance, but these activities almost never make us sick; some forms of motion sickness were recognized in which head and body motion is normal or even absent (flight simulator and Cinerama sickness).

Motion sickness: an evolutionary hypothesis.

An hypothesis is proposed suggesting that motion sickness is triggered by difficulties which arise in the programming of movements of the eyes or head when the relations between the spatial frameworks defined by the visual, vestibular, or proprioceptive inputs are repeatedly and unpredictably perturbed.

Vestibular Influences on the Autonomic Nervous System a

  • B. Yates
  • Biology, Medicine
    Annals of the New York Academy of Sciences
  • 1996
Because postural changes involving nose-up pitch challenge the maintenance of stable blood pressure and blood oxygenation in this species, vestibular effects on the sympathetic and respiratory systems are appropriate to participate in maintaining homeostasis during movement.

Motion and Space Sickness

The central Nervous Connections Involved in Motion Induced Emesis are studied and the role of Vestibular Endorgans in Experimental Motion Sickness is investigated.

Therapeutic effects of antimotion sickness medications on the secondary symptoms of motion sickness.

Ephedrine IM but not scopolamine is effective for some of the secondary effects of motion sickness after it is established, and Alterations of performance on the pursuit meter correlated with the brain wave changes.

Differences in otolith and abdominal viscera graviceptor dynamics: implications for motion sickness and perceived body position.

The potential exists for intermodality sensory conflict between vestibular and visceral graviceptor signals, at least at the mechanical receptor level, in the frequency range for motion sickness incidence in transportation, in subjects rotated about Earth-horizontal axes, and in periodic parabolic flight microgravity research.