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Related Experiment Video

Updated: Apr 27, 2026

How to Study Placebo Responses in Motion Sickness with a Rotation Chair Paradigm in Healthy Participants

How to Study Placebo Responses in Motion Sickness with a Rotation Chair Paradigm in Healthy Participants

Published on: December 14, 2014

Motion sickness: more than nausea and vomiting.

James R Lackner¹

¹Volen Center for Complex Systems, Brandeis University, Waltham, MA, 02454, USA, lackner@brandeis.edu.

Experimental Brain Research

|June 26, 2014

Summary

Motion sickness involves more than nausea and vomiting, affecting susceptibility through factors like sleep deprivation and vestibular input. Understanding its complex mechanisms is key to developing effective treatments.

Area of Science:

Neuroscience
Human Physiology
Vestibular System Research

Background:

Motion sickness is a complex syndrome extending beyond nausea and vomiting, often unrecognized in daily life.
Susceptibility varies widely, influenced by factors such as sleep deprivation and the presence of a functioning vestibular system.
Existing theories, including evolutionary and ecological models, have limitations in fully explaining motion sickness.

Purpose of the Study:

To review the multifaceted nature of motion sickness, including underrecognized symptoms and contributing factors.
To explore the role of the vestibular system and velocity storage in motion sickness.
To discuss the limitations of current theories and propose avenues for future research, including sensory conflict and visceral afferent feedback.

Main Methods:

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Using Eye-tracking to Assess the Relative Importance of Visual and Vestibular Input to Subcortical Motion Processing in the Roll Plane

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Review of existing literature on motion sickness.
Analysis of systematic studies, including those conducted in parabolic flight.
Examination of sensory conflict theory and its extensions.

Main Results:

Velocity storage of semicircular canal signals is a key factor in both space and terrestrial motion sickness.
Adaptation procedures can reduce the time constant associated with velocity storage, increasing resistance to motion sickness.
A sensory conflict theory, extended to include visceral afferent feedback, offers a broader explanation for motion sickness elicitation.

Conclusions:

A comprehensive understanding of motion sickness requires further exploration of visceral afferent contributions and the reasons behind varying conflict provocation.
Identifying the physiological mechanisms of nausea, vomiting, and anxiety is progressing, suggesting a comprehensive understanding may be attainable soon.
Currently, effective anti-motion sickness drugs without adverse side effects are unavailable.