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

1990 ◽  
Vol 68 (2) ◽  
pp. 294-303 ◽  
Author(s):  
Charles M. Oman
Keyword(s):  
Motion Sickness ◽  
General Term ◽  
Conflict Theory ◽  
Control Engineering ◽  
Sensory Conflict ◽  
Physical Motion ◽  
Vestibular Organs ◽  
The Brain ◽  
Neurophysiological Basis ◽  
Present Understanding

"Motion sickness" is the general term describing a group of common nausea syndromes originally attributed to motion-induced cerebral ischemia, stimulation of abdominal organ afferents, or overstimulation of the vestibular organs of the inner ear. Seasickness, car sickness, and airsickness are commonly experienced examples. However, the identification of other variants such as spectacle sickness and flight simulator sickness in which the physical motion of the head and body is normal or even absent has led to a succession of "sensory conflict" theories that offer a more comprehensive etiologic perspective. Implicit in the conflict theory is the hypothesis that neural and (or) humoral signals originate in regions of the brain subserving spatial orientation, and that these signals somehow traverse to other centers mediating sickness symptoms. Unfortunately, our present understanding of the neurophysiological basis of motion sickness is incomplete. No sensory conflict neuron or process has yet been physiologically identified. 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. A revised mathematical model is presented that describes the dynamic coupling between the putative conflict signals and nausea magnitude estimates. Based on the model, what properties would a conflict neuron be expected to have?Key words: motion sickness, nausea, vestibular, vision, mathematical models.

Visual Occlusion Decreases Motion Sickness in a Flight Simulator

Perception ◽  
2018 ◽  
Vol 47 (5) ◽  
pp. 521-530 ◽  
Author(s):  
Shaziela Ishak ◽  
Andrea Bubka ◽  
Frederick Bonato
Keyword(s):  
Motion Sickness ◽  
Conflict Theory ◽  
Visual Input ◽  
Simulator Sickness ◽  
Motion Platform ◽  
Visual Channel ◽  
Sensory Conflict ◽  
Sensory Inputs ◽  
Visual Occlusion ◽  
Before And After

Sensory conflict theories of motion sickness (MS) assert that symptoms may result when incoming sensory inputs (e.g., visual and vestibular) contradict each other. Logic suggests that attenuating input from one sense may reduce conflict and hence lessen MS symptoms. In the current study, it was hypothesized that attenuating visual input by blocking light entering the eye would reduce MS symptoms in a motion provocative environment. Participants sat inside an aircraft cockpit mounted onto a motion platform that simultaneously pitched, rolled, and heaved in two conditions. In the occluded condition, participants wore “blackout” goggles and closed their eyes to block light. In the control condition, participants opened their eyes and had full view of the cockpit’s interior. Participants completed separate Simulator Sickness Questionnaires before and after each condition. The posttreatment total Simulator Sickness Questionnaires and subscores for nausea, oculomotor, and disorientation in the control condition were significantly higher than those in the occluded condition. These results suggest that under some conditions attenuating visual input may delay the onset of MS or weaken the severity of symptoms. Eliminating visual input may reduce visual/nonvisual sensory conflict by weakening the influence of the visual channel, which is consistent with the sensory conflict theory of MS.

scholarly journals Contribution of intravestibular sensory conflict to motion sickness and dizziness in migraine disorders

2016 ◽  
Vol 116 (4) ◽  
pp. 1586-1591 ◽  
Author(s):  
Joanne Wang ◽  
Richard F. Lewis
Keyword(s):  
Motion Sickness ◽  
Semicircular Canals ◽  
Inverse Correlation ◽  
Normal Subjects ◽  
Otolith Organs ◽  
Rotational Axis ◽  
Vestibuloocular Reflex ◽  
Sensory Conflict ◽  
Velocity Signal ◽  
Episodic Vertigo

Migraine is associated with enhanced motion sickness susceptibility and can cause episodic vertigo [vestibular migraine (VM)], but the mechanisms relating migraine to these vestibular symptoms remain uncertain. We tested the hypothesis that the central integration of rotational cues (from the semicircular canals) and gravitational cues (from the otolith organs) is abnormal in migraine patients. A postrotational tilt paradigm generated a conflict between canal cues (which indicate the head is rotating) and otolith cues (which indicate the head is tilted and stationary), and eye movements were measured to quantify two behaviors that are thought to minimize this conflict: suppression and reorientation of the central angular velocity signal, evidenced by attenuation (“dumping”) of the vestibuloocular reflex and shifting of the rotational axis of the vestibuloocular reflex toward the earth vertical. We found that normal and migraine subjects, but not VM patients, displayed an inverse correlation between the extent of dumping and the size of the axis shift such that the net “conflict resolution” mediated through these two mechanisms approached an optimal value and that the residual sensory conflict in VM patients (but not migraine or normal subjects) correlated with motion sickness susceptibility. Our findings suggest that the brain normally controls the dynamic and spatial characteristics of central vestibular signals to minimize intravestibular sensory conflict and that this process is disrupted in VM, which may be responsible for the enhance motion intolerance and episodic vertigo that characterize this disorder.

scholarly journals Toward Predicting Motion Sickness Using Virtual Reality and a Moving Platform Assessing Brain, Muscles, and Heart Signals

2021 ◽  
Vol 9 ◽  
Author(s):  
Marco Recenti ◽  
Carlo Ricciardi ◽  
Romain Aubonnet ◽  
Ilaria Picone ◽  
Deborah Jacob ◽  
...  
Keyword(s):  
Virtual Reality ◽  
Motion Sickness ◽  
Muscle Activation ◽  
Brain Activity ◽  
Conflict Theory ◽  
Visual Signals ◽  
Physiological Factors ◽  
Biomedical Sensors ◽  
Dry Electrode ◽  
Importance Analysis

Motion sickness (MS) and postural control (PC) conditions are common complaints among those who passively travel. Many theories explaining a probable cause for MS have been proposed but the most prominent is the sensory conflict theory, stating that a mismatch between vestibular and visual signals causes MS. Few measurements have been made to understand and quantify the interplay between muscle activation, brain activity, and heart behavior during this condition. We introduce here a novel multimetric system called BioVRSea based on virtual reality (VR), a mechanical platform and several biomedical sensors to study the physiology associated with MS and seasickness. This study reports the results from 28 individuals: the subjects stand on the platform wearing VR goggles, a 64-channel EEG dry-electrode cap, two EMG sensors on the gastrocnemius muscles, and a sensor on the chest that captures the heart rate (HR). The virtual environment shows a boat surrounded by waves whose frequency and amplitude are synchronized with the platform movement. Three measurement protocols are performed by each subject, after each of which they answer the Motion Sickness Susceptibility Questionnaire. Nineteen parameters are extracted from the biomedical sensors (5 from EEG, 12 from EMG and, 2 from HR) and 13 from the questionnaire. Eight binary indexes are computed to quantify the symptoms combining all of them in the Motion Sickness Index (IMS). These parameters create the MS database composed of 83 measurements. All indexes undergo univariate statistical analysis, with EMG parameters being most significant, in contrast to EEG parameters. Machine learning (ML) gives good results in the classification of the binary indexes, finding random forest to be the best algorithm (accuracy of 74.7 for IMS). The feature importance analysis showed that muscle parameters are the most relevant, and for EEG analysis, beta wave results were the most important. The present work serves as the first step in identifying the key physiological factors that differentiate those who suffer from MS from those who do not using the novel BioVRSea system. Coupled with ML, BioVRSea is of value in the evaluation of PC disruptions, which are among the most disturbing and costly health conditions affecting humans.

A study of cybersickness and sensory conflict theory using a motion-coupled virtual reality system

Displays ◽  
2020 ◽  
Vol 61 ◽  
pp. 101922 ◽  
Author(s):  
Adrian K.T. Ng ◽  
Leith K.Y. Chan ◽  
Henry Y.K. Lau
Keyword(s):  
Virtual Reality ◽  
Conflict Theory ◽  
Virtual Reality System ◽  
Sensory Conflict

scholarly journals Interleukin-6 amplifies glucagon secretion: coordinated control via the brain and pancreas

2014 ◽  
Vol 307 (10) ◽  
pp. E896-E905 ◽  
Author(s):  
Tammy M. Barnes ◽  
Yolanda F. Otero ◽  
Amicia D. Elliott ◽  
Alicia D. Locke ◽  
Carlo M. Malabanan ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Inflammatory Disease ◽  
Interleukin 6 ◽  
Proinflammatory Cytokine ◽  
Inflammatory Diseases ◽  
Direct Action ◽  
Coordinated Control ◽  
Glucagon Secretion ◽  
The Brain ◽  
Present Understanding

Inappropriate glucagon secretion contributes to hyperglycemia in inflammatory disease. Previous work implicates the proinflammatory cytokine interleukin-6 (IL-6) in glucagon secretion. IL-6-KO mice have a blunted glucagon response to lipopolysaccharide (LPS) that is restored by intravenous replacement of IL-6. Given that IL-6 has previously been demonstrated to have a transcriptional (i.e., slow) effect on glucagon secretion from islets, we hypothesized that the rapid increase in glucagon following LPS occurred by a faster mechanism, such as by action within the brain. Using chronically catheterized conscious mice, we have demonstrated that central IL-6 stimulates glucagon secretion uniquely in the presence of an accompanying stressor (hypoglycemia or LPS). Contrary to our hypothesis, however, we found that IL-6 amplifies glucagon secretion in two ways; IL-6 not only stimulates glucagon secretion via the brain but also by direct action on islets. Interestingly, IL-6 augments glucagon secretion from both sites only in the presence of an accompanying stressor (such as epinephrine). Given that both adrenergic tone and plasma IL-6 are elevated in multiple inflammatory diseases, the interactions of the IL-6 and catecholaminergic signaling pathways in regulating GCG secretion may contribute to our present understanding of these diseases.

Modeling sensory conflict and motion sickness in artificial gravity

2008 ◽  
Vol 62 (2-3) ◽  
pp. 224-231 ◽  
Author(s):  
Paul Z. Elias ◽  
Thomas Jarchow ◽  
Laurence R. Young
Keyword(s):  
Motion Sickness ◽  
Artificial Gravity ◽  
Sensory Conflict

scholarly journals Evidence of High-Detail Perceptual Modeling in the Visual Cortex

2021 ◽  
Vol 2020 (01) ◽  
pp. 0120
Author(s):  
Terry Bollinger
Keyword(s):  
Visual Cortex ◽  
Current Model ◽  
Load Reduction ◽  
Minimal Processing ◽  
Time Model ◽  
Sensory Inputs ◽  
Physical Motion ◽  
Long Duration ◽  
Direct Corollary ◽  
The Brain

This informal but well-referenced description of an afterimage experiment called Ghost Tap provides persuasive and easily reproducible evidence that the visual cortex plays a significant role in certain classes of long-duration visual afterimages. Subjects of the experiment literally cannot discern the difference between the afterimage and reality, resulting in easy startling of the subjects when physical motion in the room no longer matches the persuasive afterimages they are perceiving. Anecdotal examples of less extreme versions of the same effect suggest that the Ghost Tap effect has, over centuries, intentionally and unintentionally helped persuade people of the existence of nominally “supernatural” effects that are just persuasive long-duration afterimages. While this description is informal, the easy reproducibility of the Ghost Tap makes it a good candidate for more precise and quantitative studies. One theory why Ghost Tap exists is that it is part of load reduction and speed enhancement strategy to compensate for the slow processing speeds of neurons. Maintaining a dynamic and predictive real-time model of likely sensory inputs from the external world would enable the brain to discard quickly and with minimal processing any sensory inputs that fall within the predictive tolerance limits to the current model state. A perceptive load reduction interpretation of the Ghost Tap argues that the ability of the brain to support dreaming in vivid detail is likely a direct corollary of its ability to create dream-like waking states for faster and more efficient processing of large sensory loads. If the brain regularly uses dream-like waking states to reduce data, more study of effects like Ghost Tap might help explain the frequency of pathologies in which perception becomes disconnected from reality.

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