Springer Series on Naval Architecture, Marine Engineering,
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Thomas G. Dobie
Motion
Sickness
A Motion Adaptation Syndrome
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Thomas G. Dobie
Motion Sickness
A Motion Adaptation Syndrome
123
Thomas G. Dobie
National Biodynamics Laboratory, College
of Engineering
University of New Orleans
New Orleans, LA, USA
ISSN 2194-8445
ISSN 2194-8453 (electronic)
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… I continue to suffer so much
from sea-sickness, that nothing, not
even Geology itself, can make up for
the misery and vexation of spirit.
—Charles Darwin, on board the Beagle
off Valparaiso, March 10, 1835
(Barlow, 1946)
About the Author
Thomas G. Dobie is Professor, Director, and Human Engineering Head of the
National Biodynamics Laboratory, College of Engineering, at the University of
New Orleans. He has also held the posts of Research Professor in Mechanical
Engineering and Clinical Professor in Psychology at the University of New
Orleans; Adjunct Professor in the Department of Cell Biology and Anatomy at the
Louisiana State University School of Medicine in New Orleans and Principal
Research Fellow in the School of Biomedical Sciences at the University of Leeds in
Great Britain.
When he was in the British Royal Air Force (RAF), he found that many keen
young flight trainees had been grounded permanently with a diagnosis of chronic
intractable airsickness, because there was no satisfactory program for dealing with
their problem. He originally developed his cognitive-behavioral anti-motion sickness desensitization training program, while serving as a medical officer (pilot) in
the RAF Flying Training Command. He was later invited as Visiting Scientist on
assignment to the Motion Sciences Department of the Naval Biodynamics
Laboratory at the University of Leeds in UK and appointed Clinical Professor in the
Department of Psychology at the University of New Orleans. At that time, he
carried out experiments designed to evaluate the key elements of his
cognitive-behavioral anti-motion sickness training program with Dr. James May,
who held the Villere Chair in Neurosciences in the Department of Psychology at the
University of New Orleans. The program was funded by the UK Admiralty
Research Establishment and the US Office of Naval Research.
He has long been intrigued by the number of famous and gallant people who
have suffered severely from motion sickness, none more so than Charles Darwin.
This complaint compelled Darwin to leave the Beagle as often as possible as he
sailed around the coast of South America, and rejoined the ship later. During these
extended journeys overland, he made many of the discoveries that led to his writing
the “Origin of Species.” He suggested to his colleague James May the possibility
that many of Darwin’s discoveries might not have been made if he had not suffered
from chronic motion sickness. Dr. May discusses this theme in the following
introduction (foreword).
vii
Foreword
In the first chapter of his work, Dobie reviews historical background and the current
definition of motion sickness and discusses the prevalence and the
physiological/psychological concomitants of the disorder. The cognitive element
appears to be crucial in his cognitive-behavioral approach, yet the physiological
reaction is obviously a result of provocative stimulation. Therefore, additions are
proposed to the physiological model of motion sickness described by Benson. This
modification offers a psychosomatic interface explaining how attitudes toward, and
memories of, motion sickness can lead to heightened arousal and emotionality. This
increases sensitivity to motion stimuli and exacerbates the effects of such stimuli.
In the second chapter, Dobie reviews the incidence of motion sickness in
numerous provocative motion environments and in Chap. 3 discusses various
personal factors that appear to influence those numbers. In Chap. 4, various characteristics of provocative motion stimuli are described, together with the results of
studies in the laboratory, motion simulators or at sea. Chapter 5 consists of an
extensive review of various physiological mechanisms underlying motion sickness
and the associated theories regarding the etiology of this malady. Chapter 6 takes
into account various psychological mechanisms that exacerbate this condition. In
Chap. 7, Dobie discusses the question of adaptation and habituation and describes
experiments to address the issue of stimulus generalization.
Attempts to circumvent the problem through careful selection of personnel did
not seem to hold much promise since the incidence of motion sickness was found to
be widespread and often occurred in individuals charged with critical tasks.
Nonetheless, as we will see in Chap. 8, considerable effort was put forth to devise
laboratory tests that might characterize an individual’s susceptibility to motion
sickness and his or her ability to adapt to motion environments. At the same time, in
Chap. 9, the author explores ways in which individuals might be trained to prevent
or cope more efficaciously with motion environments.
It was quite natural that emphasis was placed on pharmacological intervention
because this malady had for long been conceptualized as a form of sickness with
underlying physiological cause. Extensive investigation was undertaken for both
symptomatic treatments (e.g., the use of homeopathic compounds like ginger to
ix
x
Foreword
treat nausea) and pharmaceutical manipulation of the putative brain mechanisms
involved in the motion sickness syndrome. The results of these efforts are reviewed
in Chap. 10.
Programmatic evaluation of the problem became a priority in the militaries of
many countries. Multinational committees were impaneled to foster an exchange of
information, leaning heavily on what was learned from World War II regarding the
motion sickness syndrome, susceptibility, prevention, and treatment. These programs, together with Dobie’s early experiences with the management of motion
sickness, are chronicled in Chaps. 11 and 12. Studies involving measures of previous motion experience, motion sickness history, provocative tests of motion
susceptibility, and training regimens to impart adaptation to motion eventually led
to the realization that cognitive factors like emotion, memory, and motivation play
more of a role in motion sickness than was originally thought by those who conceptualized the problem as a strictly physiological reaction. A cognitive-behavioral
therapy program was developed by Dobie (1963), which sought to deal with both
the psychological attitudes toward motion environments and the adaptive processes
that occur with controlled motion experiences. This approach proved effective in
the amelioration and prevention of motion sickness. In Chap. 11, there is a review
of various desensitization programs employed in military settings and a discussion
on the relative effectiveness of those methods as compared to cognitive-behavioral
counseling. Chapter 12 offers a practical guide to the healthcare practitioner who
would consider employing this technique, including information to be covered with
the sufferer and schedules of training sessions. In addition, Dobie has also written a
more comprehensive handbook specifically for use by cognitive-behavioral
counselors.
In Chap. 13, there is a review of a series of experimental efforts in which we
collaborated to evaluate the various elements of the cognitive-behavioral approach.
The intent of these experiments was to determine which aspects of the treatment
were essential for success and how the technique might be adapted to different
settings. The results of our experiments confirmed Dobie’s conviction that the
cognitive counseling component was essential for effectiveness whereas neither
mere relaxation training with biofeedback nor behavioral desensitization with
repeated exposure to a provocative stimulus were sufficient. In addition, this
experimentation addressed the degree to which treatment under some conditions or
with some devices might generalize to other situations. Some support was found for
generalization, but the results also indicated some specificity of treatment effects.
Finally, it was determined that the cognitive-behavioral technique could be taught
easily to other counselors, was effective in their hands, and could be completed in
an optimal number of training sessions.
In Chap. 14, Dobie draws some useful conclusions from what he has learned
from his experiences while dealing with motion sickness and other medical situations in which he has employed aspects of his cognitive-behavioral technique. This
work may answer many of the reader’s questions about motion sickness, but the
author also hopes that the conceptualizations and hypotheses presented in this text
will raise many other interesting questions. There is much more to learn about
Foreword
xi
motion sickness, and we trust that the curiosity and daring that have led mankind to
develop diverse and exotic modes of transportation will also continue to spur the
scientific quests for adaptation to the side effects of those modes.
New Orleans, LA, USA
June, 2016
James G. May, Ph.D.
Preface
That Charles Darwin suffered from mal de mer (seasickness) is interesting from two
perspectives. It is worthy of note that one of the world’s great minds was subject to
this malady, but as Dobie later recounts, the list of great men who have been
similarly afflicted is extensive. It is more interesting that the current understanding
concerning the etiology of this disorder involves normal adaptive mechanisms. This
is the same general principle on which Darwin based his greatest contributions to
evolutionary theory.
In man, it is assumed that this problem is solved by integrating motion from
information provided through the eyes, ears, vestibular apparatus, and tactual
senses. In addition, we extract information about the position of our body and
limbs, while moving, from our kinesthetic receptors. During normal development,
the infant is thought to “program” each of these sensory feedback mechanisms in
the nervous system through increasingly complex motional behaviors. A natural
correspondence exists between information provided through these various sensory
channels as individuals move through a fairly static environment. For example,
visual inputs indicating movement in a given direction are associated with
vestibular and kinetic sensations for that particular direction of movement. Much
like the Venus flytrap, expectations are built which facilitate specific motor
responses, but in a much more complex and elaborate fashion.
Some researchers have termed this set of expectations concerning the correspondence between the sensory inputs the “comparator” mechanism to connote
that, through experience, the nervous system is programmed to expect correlational
inputs from the senses with regard to movement through, or of, the environment.
Given a stable environment, this comparator might evolve into an excellent adaptive mechanism for guiding movement through the world. But what if the environment changes with regard to sensory input (an earthquake occurs) or the
individual moves through the environment in a new or infrequently experienced
way, such as riding on a camel? Now, the well-ingrained expectations in the
comparator are violated with the result that adaptive compensatory movements are
more difficult to achieve. In a sense, the individual is regressed to an earlier state,
wherein the relationships between the inputs are not well learned. Successful
xiii
xiv
Preface
navigation in this new situation requires a modification or elaboration of the correspondence between inputs. Like the Venus flytrap in a more arid land, the individual becomes a victim of previous adaptation until readaptation occurs.
Our knowledge of these mechanisms is far from complete even today. Much of
what is known about motion sickness did not come from an arduous study of the
sensory inputs during motion or serious investigation of the physiology underlying
the hypothetical comparator. Rather, it grew out of the experiences of people like
Darwin, who were experiencing modes of travel for which they were not prepared.
In such situations, many individuals feel “unwell” and ascribe their malady to the
situation in which they find themselves. Initially, some researchers believed that
there were many forms of motion sickness (seasickness, airsickness, the sickness
felt on amusement park rides, etc.), and there were questions about whether the
feelings experienced by individuals in specific motion environments were the same
or idiosyncratic. Those concerned with mass transport of large numbers of people
(usually the military) began to ask how widespread the problem was and initiated
surveys to establish the incidence of the sickness associated with use of a particular
conveyance, with a view to selecting less susceptible individuals or of modifying
the vehicle to make it less likely to cause disturbance.
Acknowledgements
I wish to express my gratitude to the many people who have helped to make this
work possible. In particular, I wish to extend my profound gratitude to my friend
and colleague Dr. Jim May for all the time that we have spent discussing this
fascinating topic and in particular for writing such an erudite and interesting
introduction to this work. I also wish to thank Dr. Dennis K. McBride, Ph.D., MPA,
and President of the Potomac Institute for Policy Studies, who, as a Captain in the
United States Navy, assiduously reviewed this work on behalf of the Office of
Naval Research (ONR). I also wish to thank Commander David R. Street, Jr.,
Ed D., also of ONR, for giving his time as an independent reviewer.
In addition, I have great pleasure in thanking Ms. Lisa Johnson of the National
Biodynamics Laboratory and Mr. George R. Morrissey and Ms. Jan Felix of the
School of Naval Architecture and Marine Engineering at the University of New
Orleans for the painstaking work they have performed in editing and formatting this
work. I wish to thank my son David Dobie for coming to the rescue and remaking
and revising all of the tables and figures in the book. I would also like to thank my
eldest son Thomas Dobie for further assistance with formatting and content editing
throughout the book. I cannot thank individually the many other colleagues of
mine or the many experimental subjects who, over the years, have made all of these
efforts possible. I truly couldn't have done it without them. I only hope that the end
product will help others as they have helped me.
The opinions and interpretations contained herein are those of the author and do
not necessarily represent the views, policies, or endorsements of the Royal Air
Force, the United Kingdom Admiralty Research Department, the United States
Department of the Navy, or any other government agency.
Thomas G. Dobie OBE, MD, Ph.D., DSc
Director
National Biodynamics Laboratory
xv
Contents
1
Motion Sickness . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1.1
Definition of Motion Sickness . . . . . . . . . . . . .
1.2
Symptoms and Signs of Motion Sickness . . . . .
1.3
Physiological Responses . . . . . . . . . . . . . . . . .
1.4
Symptoms and Signs of Simulator Sickness . . .
1.5
Performance Degradation and Effect of Severity
and Motion Sickness . . . . . . . . . . . . . . . . . . . .
1.6
Sopite Syndrome . . . . . . . . . . . . . . . . . . . . . . .
1.7
A Sopite Syndrome Thesis . . . . . . . . . . . . . . .
1.8
Motion Sickness as a Stressor . . . . . . . . . . . . .
1.9
Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
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Motion .
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2
Incidence of Motion Sickness . . . . . . . . . . . . . . . . . .
2.1
Seasickness . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.2
Airsickness . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.3
Space Adaptation Syndrome . . . . . . . . . . . . . .
2.4
Simulator Sickness . . . . . . . . . . . . . . . . . . . . .
2.5
Sickness Related to Virtual Reality Systems . . .
2.6
Motion Sickness in Other Forms of Provocative
2.7
Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
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3
Correlates of Susceptibility to Motion Sickness . . . . . . . .
3.1
Motion Sickness Related to Age . . . . . . . . . . . . . .
3.2
Motion Sickness Related to the Sex of the Subject .
3.3
Why Are Females More Likely to Be Motion Sick?
3.4
Motion Sickness Related to Race or Culture . . . . . .
3.5
Motion Sickness Related to Physical Fitness . . . . . .
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xvii
xviii
Contents
3.6
Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
67
67
4
Characteristics of the Provocative Motion Stimuli
4.1
Laboratory Studies . . . . . . . . . . . . . . . . . . .
4.2
Motion Simulator Studies . . . . . . . . . . . . . .
4.3
At-Sea Studies . . . . . . . . . . . . . . . . . . . . . .
4.4
In-Flight Study . . . . . . . . . . . . . . . . . . . . . .
4.5
Parabolic Flight Studies . . . . . . . . . . . . . . . .
4.6
Underwater Studies . . . . . . . . . . . . . . . . . . .
4.7
Motion Frequencies of Concern . . . . . . . . . .
4.8
Summary . . . . . . . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
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5
Physiological Mechanisms Underlying Motion Sickness
5.1
Vestibular Overstimulation Theory . . . . . . . . . . . .
5.2
Sensory Conflict Theory . . . . . . . . . . . . . . . . . . .
5.3
Neural Mismatch Hypothesis . . . . . . . . . . . . . . . .
5.4
Visual/Inertial Rearrangements . . . . . . . . . . . . . . .
5.5
Canal/Otolith Rearrangements . . . . . . . . . . . . . . .
5.6
Vestibular/Proprioceptor Mismatch . . . . . . . . . . . .
5.7
Heuristic Mathematical Model . . . . . . . . . . . . . . .
5.8
Subjective Vertical Conflict Theory . . . . . . . . . . .
5.9
Postural Instability Theory . . . . . . . . . . . . . . . . . .
5.10 Other Intermodality Conflicts . . . . . . . . . . . . . . . .
5.11 Treisman’s Evolutionary Hypothesis . . . . . . . . . . .
5.12 Nystagmus Hypothesis . . . . . . . . . . . . . . . . . . . .
5.13 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
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6
Psychological Mechanisms That Exacerbate Motion Sickness .
6.1
Arousal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
6.2
Personality Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . .
6.3
Measured Stress Responses . . . . . . . . . . . . . . . . . . . . . .
6.4
Relationship of Salivary Gland Function to Personality
and Motion Sickness . . . . . . . . . . . . . . . . . . . . . . . . . . .
6.5
Theoretical Considerations . . . . . . . . . . . . . . . . . . . . . . .
6.6
Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
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Adaptation to Provocative Motion . . . . . . . . . . . . . . . . . . . . . . . . . 129
7.1
Protective Adaptation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 130
7.2
Mal de Debarquement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 132
Contents
xix
7.3
7.4
Adaptation—Specific or General? . . . . . . . . . . . . . . . . . . . .
Reduction of Visually-Induced Motion Sickness Elicited
by Changes in Illumination Wavelength . . . . . . . . . . . . . . .
7.5
Generalisation of Tolerance to Motion Environments . . . . .
7.6
The Transfer of Adaptation Between Actual and Simulated
Rotary Stimulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
7.7
Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Reference . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
. . 143
. . 145
. . 145
8
Prediction of Susceptibility to Motion Sickness . . . . . . . . . . .
8.1
Prevention of Motion Sickness by Candidate Selection .
8.2
Selection by Means of Motion Sickness Questionnaires .
8.3
Tests for Grading Susceptibility to Motion Sickness . . .
8.4
Comments Regarding Prediction . . . . . . . . . . . . . . . . .
8.5
Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
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9
Prevention of Motion Sickness . . . . . . . . . . . . . . . . . . . . . .
9.1
Vehicular Design . . . . . . . . . . . . . . . . . . . . . . . . . . .
9.2
General Measures . . . . . . . . . . . . . . . . . . . . . . . . . . .
9.3
The Mitigation of Specific Precipitating Factors . . . . .
9.4
Benefit of Seeing the Horizon . . . . . . . . . . . . . . . . . .
9.5
Use of an Artificial Horizon . . . . . . . . . . . . . . . . . . .
9.6
Factors Influencing Habituation to Motion . . . . . . . . .
9.7
Prevention of Motion Sickness by Vestibular Training
9.8
Factors Related to Simulator Sickness . . . . . . . . . . . .
9.9
Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
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10 Pharmacological Treatment of Motion Sickness . . . . . . . . . . .
10.1 Scopolamine (Hyoscine Hydrobromide) . . . . . . . . . . . . .
10.2 Antihistamines . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
10.3 Intramuscular Injection of Medication . . . . . . . . . . . . . .
10.4 Dextroamphetamine Sulphate (Dexedrine®) . . . . . . . . . .
10.5 Relative Effectiveness of Common Anti-motion Sickness
Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
10.6 Other Anti-motion Sickness Drugs . . . . . . . . . . . . . . . . .
10.7 Theoretical Considerations . . . . . . . . . . . . . . . . . . . . . . .
10.8 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
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11 The Use of Non-pharmacological Therapy . . . . . . . . . . . .
11.1 RAF Desensitisation Programme . . . . . . . . . . . . . . .
11.2 USAF Behavioural Airsickness Management (BAM)
11.3 USAF Biofeedback Training . . . . . . . . . . . . . . . . . .
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xx
Contents
11.4
11.5
Canadian Forces Airsickness Rehabilitation Programme . . .
US Navy Motion Sickness Prevention Programme Based on
Transfer of Adaptation . . . . . . . . . . . . . . . . . . . . . . . . . . .
11.6 US Navy Self-paced Airsickness Desensitisation (Spad) . . .
11.7 Autogenic-Feedback Training . . . . . . . . . . . . . . . . . . . . . .
11.8 Evaluation of Autogenic Training and Biofeedback . . . . . . .
11.9 Review of Military Desensitisation Programmes . . . . . . . . .
11.10 Independent Comment on Desensitisation Programmes . . . .
11.11 Other Methods Used to Treat Motion Sickness . . . . . . . . . .
11.12 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
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12 Cognitive-Behavioural Desensitisation Training—The Principles
of My Original Programme Using a Rotating/Tilting Chair . . . .
12.1 Cognitive-Behavioural Training—Historical Perspective . . .
12.2 Rationale of Cognitive-Behavioural Training . . . . . . . . . . .
12.3 Practical Application Using the Rotating Tilting Chair . . . .
12.4 First Training Session . . . . . . . . . . . . . . . . . . . . . . . . . . . .
12.5 Second Training Session . . . . . . . . . . . . . . . . . . . . . . . . . .
12.6 Type Three Training Session . . . . . . . . . . . . . . . . . . . . . . .
12.7 Type Four Training Session . . . . . . . . . . . . . . . . . . . . . . . .
12.8 Type Five Training Session . . . . . . . . . . . . . . . . . . . . . . . .
12.9 Type Six Training Session . . . . . . . . . . . . . . . . . . . . . . . . .
12.10 Type Seven Training Session . . . . . . . . . . . . . . . . . . . . . . .
12.11 Type Eight Training Session . . . . . . . . . . . . . . . . . . . . . . .
12.12 Type Nine and Subsequent Training Sessions . . . . . . . . . . .
12.13 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
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13 Experimental Evaluation of the Components
of Cognitive-Behavioural Training Using Illusory Motion
in an Optokinetic Drum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
13.1 Equipment Used for Visually-Induced Apparent (Illusory)
Motion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
13.2 UNO Optokinetic Drum . . . . . . . . . . . . . . . . . . . . . . . . .
13.3 Circular Vection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
13.4 NBDL Desensitisation Chair . . . . . . . . . . . . . . . . . . . . . .
13.5 Evaluation of Key Components of Cognitive-Behavioural
Desensitisation Training . . . . . . . . . . . . . . . . . . . . . . . . .
13.6 Counsellor Training . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
13.7 Optimal Number of Training Sessions . . . . . . . . . . . . . . .
13.8 Comparison with a Biofeedback Technique . . . . . . . . . . .
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Contents
xxi
13.9 Theoretical Considerations . . . . . . . . . . . . . . . . . . . . . . . . . . . 292
13.10 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 292
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 292
14 Overview of the Uses of Cognitive-Behavioural Training
14.1 Motion Sickness . . . . . . . . . . . . . . . . . . . . . . . . . .
14.2 High Altitude Decompression Training . . . . . . . . . .
14.3 Cardiac Catheterisation . . . . . . . . . . . . . . . . . . . . .
14.4 Tinnitus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
14.5 Theoretical Considerations . . . . . . . . . . . . . . . . . . .
14.6 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
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Chapter 1
Motion Sickness
Abstract Although motion sickness is a widespread problem that seems to have
been around forever, there is a tendency to play down its significance. There are
those who suggest that it does not play a vital role in the community as a whole or
in the military in particular. Others describe it as “wimpish” and not worthy of
attention. These attitudes are quite wrong. Motion sickness, is a motion adaptation
syndrome, that should be recognised for what it is, namely, a maladaptation to
novel provocative motion environments. It is a normal protective mechanism that
can be managed effectively if we make the effort to understand its various features.
It is also important to realise that these efforts will pay significant dividends in terms
of time and money. Those who are fortunate have an easy transition to various
forms of travel, whereas others have some difficulty in adapting to the protective
responses that are incurred. With understanding and help, these problems can be
overcome. I propose to begin this review of motion sickness by examining the very
basic aspects of this syndrome that can beset us when we venture to travel other
than on our own two feet and, when exposed to “vehicular” motion, begin to adapt
to this new world.
The problem of motion sickness has been around for thousands of years; it started
shortly after man adopted forms of travel other than his own two legs. It became
rapidly worse when he took to the water and began to travel more widely on rafts
and in canoes and boats, particularly when he became more venturesome and
headed out to sea. Reason and Brand (1975) stated that the ancient Greeks had
written on this subject and the term nausea was derived from their word naus,
meaning a ship. They also observed that Hippocrates had asserted, “Sailing on the
sea proves that motion disorders the body.” It has been reported that seasickness
was a problem for Ulysses and his compatriots in the Homeric saga, as well as the
Spanish Conquistadores and the Portuguese mariners who had sailed around the
world (Marti-Ibanez 1954). It is likely that Hannibal’s troops had suffered from
motion sickness on the backs of swaying elephants and Lawrence of Arabia was a
chronic sufferer from camel sickness. The famous British Admiral Lord Nelson
suffered from chronic seasickness, even on his last voyage to the Battle of Trafalgar.
© Springer Nature Switzerland AG 2019
T. G. Dobie, Motion Sickness, Springer Series on Naval Architecture,
Marine Engineering, Shipbuilding and Shipping 6,
https://doi.org/10.1007/978-3-319-97493-4_1
1
2
1 Motion Sickness
Many of his admirals also suffered from seasickness throughout their careers.
Charles Darwin, the distinguished naturalist hated the sea for the same reason and
suffered badly on his voyage to the coast of South America on the Beagle.
Apparently the well-known magician, Houdini, could escape from most anything
but seasickness and he had a very uncomfortable crossing when he took his act over
to Europe for a tour of magic.
In her book “All About Flying,” published in 1915, Gertrude Bacon made an
interesting observation about Louis Bleriot who built and then flew his Bleriot XI
monoplane across the English Channel from France in 1911, landing near Dover,
England. As she wrote about that flight: “Bleriot, a proverbially bad sailor, made his
first comfortable crossing the day he flew the Channel.” However, as Hallion
pointed out in his excellent book (Taking Flight 2003), Bleriot’s weather adviser
Leblanc “…had correctly predicted the air at dawn would be still and clear permitting the little airplane to fly safely.” It was probably as well that the air was so
calm on that morning, since Bleriot was so susceptible to motion sickness because
in those days these early light aircraft bounced around considerably in unstable air.
On that note, apparently the Wright Brothers’ new military airplane, the Military
Flyer, delivered to Fort Myer in 1909 “…was a reliable and easily maintained
machine, and also it had duration, though its instabilities tended to afflict both pilot
and passenger with airsickness” (Hallion 2003). Hallion further elaborated on this
particular point of the aircraft’s “bobbing and weaving” tendencies.
In Hallion’s words:
Re the bobbing and weaving: a stable airplane will hold a course “hands off.” An unstable
airplane will hold a course as long as the pilot actively keeps it in trim. If the pilot gets
slightly “behind” or “ahead” of the airplane’s motions (easily done through a variety of
factors, including control system lag and friction), he inadvertently creates a so-called pilot
induced oscillation (PIO). As shown by surviving film of its flights the Flyer clearly had a
lot of lag in its flight control system and, as a consequence, the operator clearly was often
either over or under controlling it, characterized by a “hunting” motion about all three axes.
How well I remember that problem when I was learning to fly in the Tiger Moth
which was a light biplane that was particularly prone to that form of disturbance. This
is very much a combination of turbulent weather and inadequate control of the
aircraft that can easily lead to motion sickness. As we shall see later there is a similar
problem at sea due to the interaction of the hull design and the sea conditions.
In 1975, Reason and Brand pointed out that motion sickness was particularly
difficult for the military in time of war and during many peacetime operational
emergencies; since they will require a large transit of military personnel at short
notice that degrades their performance and may create dangerous results due to
motion sickness. More recently, seasickness was found to be a particular problem
on D-Day. In his book describing the invasion, Ambrose (1994) provided vivid
images of the suffering caused by the disturbance. He summed it up with the
following observation, “Eisenhower smelled victory in the air, but to the men of the
AEI whose transports and landing craft had left harbour, the smell in the air was
vomit”. The famous American Admiral Zumwalt was plagued by seasickness
throughout his Naval career. Vice-Admiral Harry G. de Wolf who was one of
1 Motion Sickness
3
Canada’s most highly decorated officers of World War II is reported to have said
that he “never developed sea legs” and “was always seasick”. Nonetheless his
reputation for skill and daring as a Canadian destroyer Captain during the hazardous
naval operations leading up to D-Day was legendary. Whoever could have suggested that chronic motion sickness affecting a person like that was a sign that he
was in any way “wimpish”?
Not only is seasickness the commonest form of motion sickness, but also as we
shall see later, individuals vary in their susceptibility to different forms of
provocative motion. I strongly believe that this is mainly due to their introductory
experiences with these different kinds of motion. The problem is still as severe
today as it ever was, however, because many newer and equally provocative forms
of transport have been added. In addition, we now have similar problems with
today’s simulators, virtual environment systems, wide screen movies and in the
microgravity of space and no doubt there are more problems to come.
1.1
Definition of Motion Sickness
The use of the term motion sickness has been attributed to Irwin (1881) who
suggested that seasickness might better be called motion sickness because “not only
does it occur on lakes and even on rivers, but as is well known, a sickness identical
in kind may be induced by various other motions than that of turbulent water, …”.
In essence, motion sickness constitutes a maladaptation to a novel inertial environment (Steele 1968). Motion sickness has long been recognised as an unpleasant
consequence of employing some form of transportation. Tyler and Bard (1949)
described this malady as follows: “Motion sickness is a specific disorder which is
evoked in susceptible persons and animals when they are subjected to movements
which have certain characteristics”. Gay (1954) described motion sickness as a
“physical state that develops in human beings and animals when they are subjected
to oscillatory movements over which they have no control”. He suggested that the
term ‘motion sickness’ should be applied to those symptoms that develop when the
victim is being transported by means of an animal or vehicle and thereby is
detached from the Earth and in earlier days, Birren had described this situation as
follows, in 1949.
Statistically there is nothing unusual about motion sickness, since more than half of the
population may be made seasick and some investigators believe that everyone may be made
motion-sick under appropriate conditions. Motion sickness is therefore a common psychophysiological phenomenon. Animals, as well as man, share this predisposition to illness
when exposed to periodic motion. As in man, there are individual differences in susceptibility. Some dogs become motion-sick after a few minutes in a simple laboratory swing,
whereas others will not salivate and vomit even after a half hour of continuous swinging.
Before I leave the words of Birren, I wish to draw attention to the fact that he has
also described motion sickness as a “psychophysiological phenomenon.” To my
4
1 Motion Sickness
mind, this is a very important statement because this concept helps us to understand
a lot about various features of this disturbance in terms of its incidence, variability
and methods of management. None of these features of this syndrome can be fully
understood if we tackle it from a purely physiological point of view. Equally well it
would be incorrect if one were to suggest that motion sickness was “all in the
mind”. Byrne (1912) has summed up this situation very nicely when discussing the
aetiology of motion sickness. I shall also be returning to this issue many times
especially as it affects my views on the aetiology and management of motion
sickness.
In Byrne’s words:
Unquestionably the imagination plays an important part. Coupled with subconscious
memories of past experiences, it may be a powerful factor, and is always an important
secondary source of discomfort. It must not be considered, however, as the primary cause
of seasickness.
Much later, Kennedy and Frank (1984) have taken our understanding of the
aetiology of motion sickness a step further. They referred to the forms of motion
that are provocative by defining motion sickness as “a constellation of symptoms
and signs, generally adverse, due to exposure to abrupt, periodic or unnatural
accelerations.” As they pointed out, it is not produced when an individual walks,
runs or jumps, whereas propelled transportation of that individual in certain environments does produce motion sickness. As we shall see in Chap. 4, when I discuss
the characteristics of provocative motion, the provocative frequencies lie around
1 Hz, whereas we are adapted to frequencies around 8 Hz, associated with walking,
running and jumping.
This motion adaptation syndrome that we refer to as motion sickness is characterised by malaise, general discomfort, pallor, sweating, salivation, nausea and
vomiting. Provocative motion environments involve many forms of transport:
ships, small boats, aircraft, gliders, air-cushioned vehicles, trains, automobiles and
other vehicular conveyances; all of these are important to both military and commercial services. Motion sickness is also experienced in flight simulators and the
microgravity of Space Shuttle missions; and may be provoked in rotating rooms
and on rotating/tilting chairs, vertical accelerators and horizontal swings.
Additionally, motion sickness has been associated with riding on camels and elephants, but rarely on horses, a reflection of the different gait of these animals and,
therefore, the resultant frequency of the acceleration imposed on the rider. Various
forms of motion sickness have been named after the provocative motion environment or the particular vehicle involved, e.g., amusement park ride sickness and car
sickness. The characteristics of the underlying stimuli are essentially the same and
so have been the subjective responses (McEachern et al. 1942). There is no difference in the effects caused by these provocative motion stimuli, whether they
occur at sea, in the air, on amusement park rides, in an automobile, or even when
riding on a camel. It has been for this very reason that Irwin’s original suggestion
has stood the test of time and the responses have all been labeled motion sickness
(Gillingham 1966).
1.1 Definition of Motion Sickness
5
Motion sickness can also be produced in the absence of expected motion. Visual
motion alone has been sufficient to produce sickness (Dichgans and Brandt 1973),
as in the case of fixed-base simulators or when viewing wide-screen movies. This
conflicts with the description of motion sickness given by Tyler and Bard (1949) at
the beginning of this chapter. In summary, motion sickness is a response to real or
apparent motion to which a person is not adapted.
Motion sickness (or motion illness) is, however, a complete misnomer for this
response. First, the symptoms can be evoked by the absence of the expected motion
as much as by the presence of unexpected motion. Sickness associated with
wide-screen movies and simulators are examples of this. Second, the terms sickness
or illness suggest that the person involved is suffering from some kind of malady.
Although the term motion sickness is misleading, it continues to be used because,
regrettably, it has become the accepted term. This is not just a question of
semantics, however. The terms motion sickness or motion illness, by their very
nature, may well be due to the fact that the most commonly used means of management has been (and still is) pharmacological.
Observing that the question, “Is there any cure for sea-sickness?” is often posed,
Hill (1936) has pointed out that the emphasis on the word cure suggests the
presence of a pathological disorder. He reasons that whether or not motion sickness
can be regarded as normal or abnormal, there have been situations in which it is the
rule rather than the exception. Hill doubted if more than 5% of unhabituated subjects would remain entirely free from the disturbing effects of provocative motion,
assuming that the various parameters such as the range, character, duration, and
other associated features of the motion were appropriate.
Hill has further pointed out, “if we accept the definition of disease as a deviation
from the normal average condition, it follows that being prone to seasickness is the
normal condition and not a departure from it. It is, therefore, a normal response to
an abnormal environment.” The relief from motion sickness and, ultimately, the
apparent immunity that commonly occurs with practice, are also part of the normal
response. In terms of the inexperienced sailor, seasickness is the predictable
response to adequate provocative motion stimulation. Hill has stated, “there is a
world of difference between this and the equally normal response to identical
stimuli on the part of the seasoned sailor.” The process of adaptation bridges the
gap. This consists essentially in the development of a series of what Pavlov has
called “conditioned responses, whereby new nerve paths and connections are
established.” An important corollary, Hill has added, is that “whether the afferent
stimuli initiating the reflex responses of seasickness are vestibular, visceral, or
vasomotor, cerebral or cerebellar, or due to chemical changes in the blood, or to the
interaction of endocrine glands, or to some obscure cause not yet dreamt of in our
philosophy, the salutary process of adaptation remains fundamentally the same.” He
summarised this as follows: “The establishment of immunity is Nature’s cure, and
to expedite this process is the single aim of rational treatment.”
Glaser (1959) has also made an interesting observation about motion sickness:
“Motion sickness is unique among all the illnesses that afflict man. In common with
childbirth (not normally considered an illness), it can cause complete temporary
6
1 Motion Sickness
incapacitation without any pathological basis and entirely by reflex mechanisms,
though unlike childbirth it serves no obvious purpose at all.”; that is a somewhat
unusual analogy, but well said!
A person who is suffering from motion sickness is exhibiting a number of
physical signs and symptoms of a bodily disturbance; however, I also believe that
these are the result of a built-in protective response caused by exposure to
provocative motion environments for a sufficient length of time. It would be
abnormal to be incapable of exhibiting any motion sickness response. It would
perhaps be more accurate and constructive to give this disturbance the title “A
Motion Adaptation Syndrome,” although the term motion sickness will continue to
be used for the reason already given. In addition, however, one should always bear
in mind that in some cases the cause of sickness associated with motion could be
primarily psychological and entirely unrelated to the motion profile, since nausea
and vomiting are common reactions to stressful situations in certain types of personality (Gellhorn and Loofbourrow 1963).
1.2
Symptoms and Signs of Motion Sickness
Cardinal Indicators: The main symptom of motion sickness is nausea and the
main signs are pallor, sweating and vomiting. There are many other responses that
have been reported to varying degrees, such as apathy, general discomfort, headache, stomach awareness, increased salivation and prostration. Other, less common
manifestations include drowsiness, frontal headache and hyperventilation (Money
1970). It is interesting to note that drowsiness may not be as uncommon as some
have suggested. Indeed, Graybiel and Knepton (1976) have referred to it as one of
the cardinal symptoms of motion sickness. They have proposed that drowsiness and
mental depression are part of a symptom-complex that they have chosen to call the
“Sopite Syndrome”; this is not yet a definite form of motion sickness and will be
discussed later in this chapter. Motion sickness responses usually develop in a fixed
order over a varying period of time, based upon personal susceptibility and the
severity and duration of the stimulus.
Although Tyler and Bard (1949) pointed out that the symptoms and signs of
motion sickness varied in number and severity among individuals, they believed
that on the average, their onset followed an approximate order of appearance. First
was drowsiness, which might indicate a change from an initial pleasant response to
motion to a feeling of illness. Then came facial pallor and cold sweating which they
considered to be the most reliable indicators of motion sickness. Next, they listed
increased salivation accompanied by swallowing, followed by nausea associated
with stomach awareness and finally vomiting. They also pointed out that the
severity of incapacitation varied widely and might or might not be related to the
occurrence of vomiting. In their view, headache and dizziness were too vague to be
considered useful predictors.
1.2 Symptoms and Signs of Motion Sickness
7
Benson (1988) also supported the idea that symptoms and signs generally
developed in a common sequence, but he put forward a somewhat different order.
Beginning with stomach awareness, he then followed with the onset of nausea of
increasing severity. At the same time as nausea began, he suggested that other
symptoms and signs became evident, namely, facial pallor, cold sweating, increased
salivation, sensation of bodily warmth, light headedness, depression and apathy;
sufferers would soon either vomit or experience prolonged nausea.
Turner and Griffin (1995) investigated the incidence and characteristics of the
motion sickness responses of crewmembers during the British Steel Challenge
round-the-world yacht race; I shall also refer to various other aspects of that study
later in this book. The crewmembers were requested to rate the frequency of
occurrence of 14 different signs or symptoms of motion sickness (responses) in
their post-race reports, using a 4 point scale, as follows: (0) = response never
experienced; (1) = response occasionally experienced; (2) = response often
occurred; and (3) = response always occurred. The most commonly reported
response was nausea and others, in decreasing order of frequency, were: a sensation
of bodily heat, sweating, apathy and fatigue. Following a factor analysis of the
response frequency data, these researchers extracted four factors. The majority of
the variance has been explained by the “principal nausea” factor. In addition, all of
the recorded responses were closely related to their associated factors. The incidence of the various signs and symptoms (responses), together with the associated
factors and percentage variance are shown in Table 1.1.
Table 1.1 Distribution of motion sickness symptoms and signs experienced during the British
Steel Challenge yacht race with factor analysis groupings (post-race assessment N = 99)
Factor
Motion sickness
variance explained (%)
Symptoms and
signs (responses)
Crew members
experiencing response
(%)
Principal
nausea
45.3
Head
symptoms
10.8
Respiratory
8.4
61
56
48
47
34
49
37
31
19
49
36
11
Tiredness
7.2
Nausea
Heat sensation
Vomiting
Apathy
Retching
Fatigue
Headaches
Tension
Dizziness
Sweating
Increased salivation
Breathing
irregularities
Yawning
Drowsiness
Adapted from Turner and Griffin (1995)
34
33
8
1 Motion Sickness
Later on in this chapter, when I discuss the signs and symptoms of simulator
sickness, readers will find that Kennedy et al. (1990a) described three major
symptom clusters based on subjective reports of motion sickness symptoms. These
were: “visual” (eyestrain, focusing problems, blurred vision and headache), “vagal”
(nausea, stomach awareness, increased salivation and burping), and “vestibular”
(dizziness and vertigo). It is not surprising to find some differences in these three
sets of data when one takes into account the nature of the tasks. Simulator training
involves more visual effort than handling a yacht.
Reason and Brand (1975) described these responses as the most commonly
reported signs of motion sickness, along with vomiting. They also pointed out that
the signs of pallor were usually first seen around the nose and mouth (known as
circumoral pallor). They also tried to ‘acclimatise’ one highly susceptible subject
who suffered from chronic motion sickness by repeated daily exposure to motion
for twenty-three successive days and although that built up a degree of tolerance, it
was unsuccessful; another example of the failure of behavioural-only training!
Morton et al. (1947) have reported on the symptoms and signs of motion
sickness in 175 naval ratings and 42 other subjects who were exposed to
provocative motion on their “Roll and Pitch Rocker,” designed to simulate ship
motion, and described further in Chap. 4. These motion responses are shown in
Table 1.2. In general, the incidence of these symptoms, for subjects whom Morton
et al. would have classified as “miscellaneous,” is similar to those obtained during
provocative motion experiments on the motion simulators at the National
Biodynamics Laboratory (NBDL). Stomach (epigastric) awareness, which is an
uncomfortable sensation in the pit of the stomach, is certainly a common early
symptom of motion sickness. If exposure to the provocative stimuli continues,
nausea usually follows soon after. This is often associated with facial pallor and
cold sweating.
Pallor: Harm (1990) has reported on the physiology of skin pallor and pointed
out that the neural control of these mechanisms is sympathetic adrenergic in origin.
On the one hand, an increase in sympathetic activity causes pallor, whereas
Table 1.2 Incidence of
symptoms produced by an
experimental “roll and pitch
rocker”
Symptoms/Signs
175 ratings
(%)
42 misc. subjects
(%)
Epigastric
awareness
Pallor
Malaise
Nausea
Vomiting
Sleepiness
Yawning
Headache
Sweating
Abdominal cramps
Salivation
48
60
47
42
43
30
19
18
17
17
2
2
43
45
57
33
14
28
21
21
7
21
1.2 Symptoms and Signs of Motion Sickness
9
inhibition or withdrawel of such activity causes flushing. Crampton (1955)
attempted to elicit motion sickness in 22 volunteers using a type of elevator that
exposed the subjects to a symmetrical wave form in heave. The amplitude was 7′6″
at 15.6 cpm, with a mid-wave velocity of 400′ per/min. Seven of the subjects did
not reach the stage of becoming nauseous, whereas five became nauseated and the
remaining 10 subjects vomited. Facial pallor was measured by sampling colour
slides for each subject. These slides were ranked according to the severity of the
pallor. That produced a measure of “pallor change” since the ratings had not
provided an absolute measure. The pallor responses of the subjects in the three
groups were related to the duration of exposure to provocative motion (Table 1.3).
Based on that study, Crampton concluded that in most subjects the only common
sequence of responses had been the onset of pallor, followed by nausea and
vomiting; other motion sickness responses showed a wide variation between subjects; at the National Biodynamics Laboratory we are becoming very interested in
pallor measurements. Researchers have relied heavily on measures of the severity
of motion sickness based on questionnaire responses. It would be a big step forward
to be able to obtain reliable physiological measures, such as pallor, as our yardstick.
Table 1.3 Motion
stimulation time, in minutes,
to the onset of pallor, nausea
and vomiting
Subject
No.
Not sick
Pallor
Nausea
Vomiting
132
None
None
None
117
30
None
None
133
None
None
None
110
45
None
None
122
35
None
None
83
None
None
None
140
None
None
None
Nausea
221
20
38
None
only
212
36
37
None
103
27
29
None
210
16
24
None
16
None
33
Nonea
Vomiters
106
20
23
57
49
16
18
55
201
16
17
47
136
14
18
31
138
15
16
24
204
14
12
18
50
10
11
14
b
4
13
113
101
4
4
12
102
8
9
11
a
The camera jammed at the 17th min no further pictures were
available
b
Pictures for the first 5 min were fogged
10
1 Motion Sickness
Cold Sweating: This response can be defined as sweating in the absence of an
adequate thermal stimulus (Hill 1936). It occurs in areas of the skin that are usually
associated with thermal sweating rather than with sweating caused that is caused by
emotional disturbances. However, McClure et al. (1971) have reported a different
distribution of cold sweating, namely a palmar (arousal) response, that is associated
with the first two head movements during exposure to Coriolis stimulation. Coriolis
stimulation refers to the stimulation of the individual’s semicircular canals that
occurs when he or she moves his or her head other than in the imposed plane of
rotation, while being rotated about a particular axis. As the stimulation continues,
this sweating reaction due to arousal quickly decays and is replaced by a clear
response from the areas usually associated with thermally-induced sweating. They
have suggested that this early response is not part of the motion sickness syndrome,
but represents the “orientation reaction” suggested by Lynn (1966). My colleagues
and I (Dobie et al. 1989) have witnessed a similar transient arousal when subjects
have been exposed to unfamiliar stimulation caused by changing illumination
wavelength during visually-induced apparent motion. This topic will be discussed
in more detail later, in Chap. 7, when I shall be reviewing the subject of adaptation
to provocative motion.
Hemingway (1944) studied cold sweating in man caused by motion that
involved changing linear and centrifugal accelerations varying between 1.0 and
2.0 G; fit male subjects between the ages of 20 and 30 years took part. The study
used a galvanometric device to indicate the onset of sweating. He pointed out that
cold sweating is associated with mental stress and exposure to provocative motion.
In this experiment, the onset of motion sickness was not associated with any
significant anxiety. Subjects who were susceptible to provocative motion usually
showed motion sickness responses within 20 min. The sweating was found to result
from the response to provocative motion and a fall in oral temperature. This rapid
onset of cold sweating resulting from the effects of a usual vestibular stimulus was
also confirmed by a study at the US Naval Medical Institute at Pensacola.
In terms of motion sickness, Hemingway saw no useful physiological purpose in
cold sweating. He reasoned: “the motion sickness syndrome is probably a primitive
defense mechanism in which the reaction to a harmful stimulus is emesis.” A
similar reaction has been reported from other types of stress, such as brain injury,
pregnancy and the ingestion of digitalis (Hatcher and Weiss 1922) as well as in the
presence of staphylococcus enterotoxin (Bayliss 1940). In the case of motion
sickness, however, the response is a result of exposure to a new motion environment to which the subject has not yet become accustomed and a protective response
seems reasonable.
Many different stimuli have been effective in producing the characteristic train of
symptoms but “the motor mechanism is the same for all.” Hemingway (1944) has
stated that whether emesis results from a poisonous drug or from injury to the
gastrointestinal tract, it is reasonable to explain this reaction as a logical defense. He
has questioned why emesis together with cold sweating resulting from motion
would be a useful protective mechanism. Hemingway concluded that some
explanation, perhaps based on “evolutionary development” was needed. Treisman
1.2 Symptoms and Signs of Motion Sickness
11
(1977) proposed such a theory, and this will be discussed later, in Chap. 5, when
we are discussing physiological mechanisms that underlie motion sickness.
Warwick-Evans et al. (1987) observed that, in the absence of thermal stimulation, sweating is one of the cardinal symptoms of motion sickness. They proposed
that this response might have value as an index of the severity of motion sickness
since sweating bears a close relationship to electrodermal activity. In order to
evaluate this hypothesis, they carried out four experiments to examine the correlations between electrodermal activity and a range of signs and symptoms of motion
sickness. A total of 170 subjects were exposed to Coriolis stimulation. The
researchers found that increases in skin conductance did not correlate with particular individual indicators of motion sickness. They noted, however, that correlations with a motion sickness questionnaire based on several signs and symptoms of
this malady varied widely from significant to non-significant. Warwick-Evans and
his colleagues then concluded that skin conductance possibly offered a valuable and
accurate measure of motion sickness. Nevertheless, they also pointed out that “it is
sensitive to extraneous factors, only some of which are currently understood.”
Electrodermal Activity: Isu et al. (1987) have investigated the qualitative
relationship between changes in electrodermal activity and the severity of motion
sickness, as well as the association between the onsets of these responses. They
recorded the skin potential level and skin resistance level in both the arousal and
thermal sweat areas while inducing motion discomfort either by means of Coriolis
stimulation and/or horizontal body rotation, on a rotating chair. The severity of
motion sickness was evaluated by means of subjective estimations. Isu et al. found
that the skin potential level depolarised in both the arousal and thermal sweat areas.
Skin resistance level decreased in the thermal sweat area during the time that
motion discomfort lasted. Skin potential level corresponded better with lasting
symptoms than did skin resistance level, especially during the recovery period.
However, lower skin potential levels have not always been a good indicator of
motion discomfort. Additionally, they reported that sound stimulation has lowered
subject skin resistance levels, but has caused a rise in subjective arousal.
Golding (1992) noted that there were many attempts over the years to relate
sweating, or associated electrodermal activity, to the severity of motion sickness.
He pointed out that Isu et al. (1987) and McClure et al. (1971) carried out the most
comprehensive studies due to the fact that they had compared recordings from both
palmar and non-palmar sites. Golding tried to improve the technique used in these
experiments by studying both the choice of recording site (namely, the palmar
aspect of the finger versus the forehead) and the method of signal analysis (tonic
versus phasic activity). He aimed, therefore, to optimise the use of the skin conductance responses as an indication of the severity of motion sickness. He exposed
11 subjects to Coriolis provocative motion involving active head movements performed at a rate of 16 per minute during rotation around the Earth vertical axis. The
speed of rotation was increased by means of a staircase profile from 3° to 99°/s until
the subjects experienced moderate nausea. Six of the subjects were tested under
additional control conditions during which they experienced only rotation or only
head movements. Another group of 12 subjects was exposed to sessions of vertical
12
1 Motion Sickness
and horizontal sinusoidal linear motion through the z-axis of the head at 0.3 Hz,
1.8 m/s/s root-mean-squares (rms). Sweat production was recorded in a further 3
subjects, using a dry nitrogen gas flow method of mass spectrometry, in order to
measure the loss of water vapour from the skin.
Golding found that during provocative motion, skin conductance responses
showed significant effects for time, marginal effects for site and a significant time x
site interaction. When he examined the means, Golding observed that the source of
these effects was the rise in skin conductance at the forehead, but not at the fingers,
with a rise in motion sickness ratings and a subsequent drop during recovery.
Golding concluded that skin conductance activity at the forehead site provided the
best correlation with motion sickness and recovery.
Homick et al. (1984) reported that astronauts in the Space Shuttle Programme
experienced episodes of emesis that were unaccompanied by the usual prodromal
signs of motion sickness. This caused Lackner and Graybiel (1986) to ask themselves whether space motion sickness was different from terrestrial motion sickness.
The goal of this report was to summarise the systematic data on sudden emesis from
parabolic flight studies of aetiological factors in space motion sickness. While
studying parabolic flight experiments in a Boeing KC-135 aircraft, they found that
more than 60 of the greater than 300 subjects tested had sudden vomiting without
prior symptoms of motion sickness. Each subject experienced at least 4, and up to a
maximum of 64, 40-parabola flights. These workers also presented data concerning
emesis on landing, during which the sudden deceleration of the aircraft caused
provocative vestibular stimulation. They reported that this single marked vestibular
stimulation could have caused sudden emesis following exposure to low-grade
stimulation in flight. They also noted that this experience was not unpleasant, was
short lived and could occur without any prior symptoms in flight. In subjects who
had prior symptoms of motion sickness, the most common pre-existing symptoms
included stomach awareness and stomach discomfort; pallor and nausea were less
common. Perhaps there had been insufficient time for these physiological disturbances to occur. Also, most of the subjects found that emesis gave immediate relief
and was not associated with nausea. They also noted that sudden emesis could
occur following provocative vestibular stimulation on Earth, similar to space flight.
Lackner and Graybiel concluded that this particular sign of sudden emesis without
the usual escalation of symptoms, didn’t differ much whether in space or on the
ground.
Chronic Responses: As the symptoms of motion sickness rapidly increase, there
may be increased salivation and the sufferer may feel warm, lightheaded and
apathetic. When this stage has been reached, vomiting usually occurs in a short
time, although some people remain severely nauseated for a long time without
retching or vomiting. Vomiting may or may not offer relief of symptoms. If
vomiting becomes severe and repeated, it can lead to dehydration and the loss of
electrolytes. This may have serious consequences, quite apart from the metabolic
disturbances, including a significant loss of body weight. A number of 19th century
physicians have described the effects of seasickness. For example, de Zouche
1.2 Symptoms and Signs of Motion Sickness
13
(1894) has meticulously recorded the various serious manifestations associated with
chronic seasickness.
In de Zouche’s words:
In the majority of cases a favorable reaction takes place without further symptoms, the
vomiting and nausea cease spontaneously, a ravenous appetite succeeds, and the patient
feels well. In other instances great exhaustion supervenes rapidly or gradually. The patient
feels miserably helpless. He suffers from coldness of the extremities, thirst, headache, and
spasmodic pain in the stomach, and complains of numbness of the surface of the body.
There is frequently a great tendency to heavy sleepiness; and vomiting of gastro-biliary
fluids, sometimes mixed with striæ of blood, takes place whenever they collect in the
stomach. A semi-comatose condition, from which the patient is with some difficulty roused,
is sometimes met with in very severe cases, and requires assiduous treatment. In these
prolonged cases reaction may assume a febrile character, with a rapid pulse, flushed face,
hot skin, and urine containing lithates; and convalescence is slow.
Some two years later, DePuy (1896) recorded additional information on this
subject: “Along with the sickness there is a great physical prostration, as shown in
the pallor of the skin, cold sweats, and feeble pulse, accompanied with mental
depression and wretchedness.”
During a survival situation, such as on a life raft, these mental symptoms of
chronic seasickness lower morale, cause loss of interest in the surroundings and
lack of co-operation during rescue attempts. In carrying out an analysis of sea
survivors, Llano (1955) noted that many became so apathetic due to mental
depression associated with their seasickness, they failed to respond to search aircraft
overhead and consequently were presumed dead (see Table 1.5).
1.3
Physiological Responses
Morton et al. (1947) recorded ECG records obtained from 23 subjects of whom 13
became sick due to provocative motion. They did not find a constant change in
heart rate nor the PQRST complex due to the motion. In 12 of the subjects who had
experienced motion sickness, the heart rate increased by an average of 6 beats per
minute, and in 10 subjects who had not become sick, the average rate had been
reduced by the same amount. Respiratory rate and rhythm was recorded on 22
subjects and there was little change other than a slight reduction in rate and frequent
sighing. One subject who had developed tetany due to hyperventilation had shown
an increase in respiratory rate from 13 to 34 breaths per minute and heart rate from
96 to 148 beats per minute. Blood pressure had been recorded in 4 subjects and no
changes were noted before, during or after exposure to motion. The
electro-encephalographic records from 23 subjects showed no consistent change in
those subjects who became sick. In all of these 23 subjects, the alpha waves showed
damping early in exposure to provocative motion, which they had associated with a
moderate degree of early anxiety.
Morton and his colleagues reported on investigations they carried out to evoke
motion sickness in animals using a simple swing. They found that cats were
14
1 Motion Sickness
unsuitable since vomiting only occurred 3 times in a series of 14 experiments with 6
animals. Whereas, in 35 experiments that exposed 20 dogs to a simple swing
stimulus, vomiting occurred in 26 cases (74%); one wonders if this reflects the cat’s
greater agility, with resulting adaptation to that type of motion.
Lackner and Graybiel (1980) have evaluated the relationship between the
symptoms of motion sickness and the responses in terms of blood pressure, heart
rate and body temperature; In this study, they used the sudden-stop visual vestibular
interaction test (SSV in Chap. 8), to examine whether there had been a consistent
relationship in the responses of individual subjects over repeated tests. They
reported that there were no systemic changes in the physiological parameters, either
within or across subjects, with increasing severity of motion sickness. Next they
carried out a further analysis in an attempt to identify any possible trends. In this
part of the study, they tabulated the numbers of subjects across sessions showing
increases, decreases or no apparent changes in blood pressure, heart rate and body
temperature when the symptoms of motion sickness were increased from baseline
(no symptoms) to epigastric awareness; from awareness to epigastric distress; and
finally, epigastric distress to nausea. In the few cases where a particular symptom
had not been reported, however, the transition to the more severe level; had been
used, the results are in Table 1.4.
It can be seen that heart rate recorded in that table has been remarkably constant
at different levels of severity of motion sickness, whereas blood pressure and body
temperature were much more labile and might increase or decrease. None of the
changes in the physiological parameters that have been associated with changes in
Table 1.4 Direction of changes in blood pressure, heart rate and body temperature associated
with changes in motion sickness symptomatology, across subjects and sessions
Physiological measure
Blood pressure (systolic)
Changes in symptomatology
BL
EAa (%)
EA
ED (%)
ED
Increase
16
40
22
48.9
19
39.6
Decrease
19
47.5
13
28.9
22
45.8
5
No change
Blood pressure (diastolic)
Heart rate
Body temperature
N (%)
12.5
10
22.2
7
14.6
Increase
12
30
21
46.7
17
35.4
Decrease
16
40
19
42.2
20
41.7
No change
22.9
12
30
5
11.1
11
Increase
1
2.5
3
6.6
1
2.1
Decrease
1
2.5
0
0
1
2.1
No change
38
95
42
93.4
46
95.8
Increase
10
25
14
31.9
10
21.3
Decrease
16
40
17
38.6
18
38.3
No change
14
35
13
29.6
19
40.4
BL baseline, EA epigastric awareness, ED epigastric distress, N nausea
a
In 8 of the 48 experimental sessions epigastric awareness was not experienced and in three sessions
epigastric distress was not experienced; in one of subject JD’s sessions, body temperature was not
recorded
1.3 Physiological Responses
15
the severity of motion sickness were found to be significant. Consequently they
concluded that the physiological parameters by themselves were not adequate
indices of an individual’s severity of symptoms of motion sickness.
Steele (1968) was of the opinion that the most significant symptoms of motion
sickness seem to have been caused by a reduction in the volume of the circulating
blood. He described an individual who was shown to be susceptible to provocative
motion as demonstrating features of a pre-collapse state as indicated by a sharp drop
in his systolic blood pressure and minute volume, despite increasing arterial
peripheral resistance. He further reasoned that the body’s own indication of inadequate blood circulation is shown by an increase in the output of antidiuretic
hormone. Steele also pointed out that stimulation of the V111th (vestibule-cochlear)
nerve caused a fall in blood pressure that could be blocked by cutting the vagus
nerve and that stimulating the peripheral cut end of that nerve caused a similar
reduction in blood pressure.
Reason and Brand (1975) pointed out that quite a number of attempts had
previously been made to identify electroencephalographic (EEG) changes associated with susceptibility to motion sickness, but these have met with little success;
for example, Cipriani and Morton (1942) didn’t find any changes after swinging
human subjects. But in 1950 Chinn et al., on Board a US Army Transport found
that seasickness caused an activation of the alpha-rhythm and an associated slowing
of the dominant wave frequency. They also found that an EEG pattern that suggested drowsiness was evident in persistent or chronic motion sickness. They also
cited Jasper and Morton (1942) and Lindsley and Wendt (1944) who had tried
unsuccessfully to find any systematic correlates between the characteristics or the
aberrations of a subject’s EEG traces and their susceptibility to motion sickness.
Overall it was concluded that EEG changes by themselves could not be used as a
means of pre-selecting aircrew candidates who were susceptible to airsickness.
Reason and Brand (1975) and Money (1970) reported on various physiological
correlates associated with motion sickness summarised by Nicogossian and Parker
(1982) in Table 1.5. For example, prior to WW 11 blood pressure and pulse-rate
studies during seasickness were made by many investigators but the evidence was
unreliable and of little value. They later found that respiratory changes were not
consistent either. In 1943 Schwab examined many in hospital suffering from
chronic seasickness. About 50% seemed to have abnormalities in their
gastro-intestinal tract, detected by barium fluoroscopy. There was a large amount of
agreement amongst the findings in the field of gastrointestinal changes that
developing acute motion sickness showed a reduction of gastric motility and a
relaxation of the visceral involuntary muscles, but the cause of the nausea was not
specific. They noted that Birren had claimed that no correlation was found between
the anatomical and functional aspects of the gastro-intestinal tract and sickness. So
Birren concluded: “… the response of the gastro-intestinal tract in motion sickness
is not significantly influenced by differences in the characteristics of these organs.”
In 1955, Crampton found only small differences in the gastro-intestinal records
of sick and non-sick subjects when he used an intragastric recording device.
However, one of the problems was that any effect, at least partly, might be due to
16
1 Motion Sickness
Table 1.5 Physiological correlates associated with motion sickness
Physiological
systems
Responses
Cardiovascular
Changes in pulse rate and/or blood pressure
" Tone of arterial portion of capillaries in the nail bed
# Diameter of retinal vessels
# Peripheral circulation, especially in the scalp
" Muscle blood flow
Alterations in respiratory rate
Sighing or yawning
Inhibition of gastric intestinal tone and secretions
Salivation
Belching
Epigastric discomfort or awareness
Sudden relief from symptoms after vomiting
Changes in LDH concentrations
" Hemoglobin concentration
" pH and # PaCO2 levels in arterial blood, presumably from
hyperventilation
# Concentration of eosinophils
" 17-hydroxycorticosteroids
" Plasma proteins
" 17-hydroxycorticosteroids
" Catecholamines
# Body temperature
Coldness of extremities
Ocular imbalance
Dilated pupils during emesis
Small pupils
Apathy, lethargy, sleepiness, fatigue, weakness
Depression and/or anxiety
Mental confusion, spatial disorientation, dizziness, giddiness. Anorexia,
unusual sensitivity to repulsive sights or odors, or excessive discomfort
from previously tolerable stimuli such as heat, cold, or tightness of
clothing
Headache, especially frontal headache
# Muscular coordination and psychomotor performance
# Time estimation
# Motivation
Respiratory
Gastrointestinal
Body fluids,
blood
Urine
Temperature
Visual system
Behavioral
the presence of the device, when introduced into the gastro-intestinal tract, rather
than the experimental treatment itself. Recently this problem has been overcome by
the use of external recording methods for measuring gastro-intestinal potentials, the
electrogastrogram or ECG (Davis et al. 1932). He did, however, notice rather abrupt
rises and falls in gastric tone during acceleration on the vertical oscillator, but there
wasn’t a correlation between these changes in tonus and either nausea or vomiting.
1.4 Symptoms and Signs of Simulator Sickness
1.4
17
Symptoms and Signs of Simulator Sickness
Some evidence has been gathered suggesting that the pattern of symptomatology
may vary according to the type of stimulus. For example, Kennedy et al. (1990b)
described simulator sickness as “a constellation of motion-sickness-like symptoms
and signs with slightly different patterns or profiles from ‘true’ motion sickness.”
By that statement, they emphasised their view that in simulator sickness those
disturbances that relate to vision have been more common than gastrointestinal
responses. They have referred to Casali’s (1986) observation that the term “motion
sickness” is not an appropriate description for sickness caused by simulators since
many simulators do not involve physical motion. Instead, the user experiences the
visual perception of motion. Most of the classical symptoms and signs that we
associate with motion sickness have, however, been described in relation to simulators. It has been reported that in the relatively rare event that vomiting does
occur, it can do so without prodromal nausea. This is similar to a situation that has
been described by astronauts suffering from space adaptation syndrome. Following
simulator sessions, numerous after-effects have been experienced. These have
included postural changes and illusions of climbing and turning and in some cases,
disorientation.
Kennedy et al. (1990a) have also observed that instructor pilots are more susceptible to these after-effects than are the students. Money (1991) has also noted
that the incidence of simulator sickness is commonly higher in pilots who have
relatively little experience with the relevant simulator. He has further pointed out
that it seems to be even higher among pilots who have considerable experience with
the actual aircraft and at the same time have relatively little experience with the
simulator; similar to my findings later with the LCAC’s.
This is also similar to a situation that I had noticed when carrying out
cognitive-behavioural anti-motion sickness training in the RAF. Two flight
instructors who had been interested in sending students into that programme visited
the training site and asked to experience the Coriolis stimulation provided by the
rotating/tilting chair used in the desensitation part of the programme. The duration
of the demonstration exposure was short and they had not experienced any motion
sickness responses whatever. After an hour or so, they flew back to their base. Both
of these individuals subsequently reported experiencing disorientation on that flight.
It had been mild and uneventful, but certainly it was unlike any reports from the
student aviators who had been undergoing cognitive-behavioural training.
The observation that experienced people tend to be more affected by provocative
stimulation than those who are inexperienced would seem to be contradictory.
Perhaps the significant aspect is familiarity with a particular situation. The experienced aviator, for example, is comfortable with his aircraft, but less so in the
unfamiliar environment of simulation. When I visited the LCAC crews I had
observed a similar situation with experienced LCAC (landing craft air cushion)
crewmembers and students. The experienced individuals tended to have more
simulator sickness and less motion sickness on the vessel at sea, whereas the reverse
18
1 Motion Sickness
was the case for the trainee population, they were more sick at sea than on the
simulators; or was it a reflection of the fact that young trainees had more experience
with electronic games?
Kennedy et al. (1991) have elaborated on the observation that many of the
symptoms of simulator sickness are the same as those that occur in motion sickness
generally, including nausea, sweating, disorientation and drowsiness. In addition,
these workers have stressed that, unlike motion sickness, simulator sickness produces visual dysfunction. This has included reports of eyestrain, blurred vision,
difficulty in focusing and a sudden recurrence of previous symptoms (flashbacks).
Money (1991) has speculated that simulator sickness is only a part of what we
usually regard as motion sickness. He opined that the gastrointestinal symptoms
that have been reported are probably those of motion sickness, including stomach
awareness and nausea induced by a conflict in the sensory input relating to orientation and motion. However, he believed that there were additional separate
visual and vestibular phenomena in the description of simulator sickness. Older
simulators without visual displays or small dark displays produced virtually no
motion sickness. He suggested that the introduction of larger wide-angle visual
displays produce self-motion and that they stimulated the visual system in such a
way as to provoke the vestibular system, presumably by inducing a pattern of
activity that includes either conflict or mismatch in the vestibular centers. He also
noted that as simulation has improved, simulator sickness has become a greater
problem. Money has pointed out that modern simulators have a motion base and
their mechanical responses may well initiate motion sickness, particularly if they
are lower in frequency. Simulators cause visual inputs which are both imperfect in
depth and which vary with the position of the pilot’s eyes as he moves his head.
Money has introduced the interesting and important point that simulators are
commonly test situations and therefore stressful. He has summarised simulator
sessions as being lengthy, stressful and tiring, whether or not they provoke any of
the common symptoms of motion sickness. Money has also referred to the fact that
headaches are common in simulators and these could come from various origins,
namely, as a symptom of motion sickness, due to less than accurate visual displays
or heavy workload. In similar fashion, the drowsiness commonly reported could be
either motion sickness or merely a reflection of the lengthy and high intensity
workload.
Frank et al. (1983) have noted that, in addition to the symptoms experienced
while “flying” the simulator, the associated psychophysiological disturbances can
last for several hours after the experience, or the onset can be delayed until the
exposure is completed. They have found that the effects occur in motion and fixed
base simulators and affect pilots, other aircrew and instructors. These workers have
also reported that the symptoms of simulator sickness include disorientation,
dizziness, nausea, emesis, spinning sensations, motor dyskinesia, flashbacks, visual
dysfunction, burping, confusion and drowsiness.
They have recognised that the adverse effects of simulator sickness can be
considered in three main categories. First, the symptoms of simulator sickness
might interfere with the effectiveness of training in the simulator because of the
1.4 Symptoms and Signs of Simulator Sickness
19
onset of those symptoms. If the processes learned in the simulator were not the
same as those learned in flight, it would constitute negative transfer to the conditions of flight. Second, the severity of simulator sickness could well lead to a
reduction in simulator usage or confidence in the effectiveness of the training that is
provided by the simulator. Third, the after-effects of the discomfort of simulator
sickness might well have potentially hazardous effects in terms of safety as they
affect, for example, the subject’s ability to drive. This could also have an impact in
terms of other skilled and potentially hazardous tasks, such as flying. The presence
of sickness during simulation, but not in the real aircraft, suggests bad simulation.
Such a situation could then lead to motivational problems, diminished or inefficient
training or post-run hazards.
In 1993, Kennedy et al. developed a new simulator sickness questionnaire to
meet three major aims. Their first aim was to provide a more appropriate index of
simulator sickness as distinct from motion sickness. Their second aim was to
provide specific subsets of symptoms that created a significant problem. That was
intended to provide better indicators of the cause of that particular simulator
sickness. Their third aim was to provide some means of scoring the progress of
simulator sickness in order to better record and follow the progress of these
responses.
These workers have pointed out that their aim has been to identify symptoms
that showed systematic changes from pre- to post-exposure, those that have been
recorded so infrequently as to be of little or no value as statistical indicators and
those that did not change in frequency or severity. These various symptoms were
then eliminated from further analysis. They then carried out three-, four-, five- and
six-factor solutions from the 16 symptoms that remained from their original list.
They found that the three-factor solution demonstrated those three clusters that they
labeled “visual” (eyestrain, focusing problems, blurred vision and headache),
“vestibular” (dizziness and vertigo) and “vagal” (nausea, stomach awareness,
increased salivation and burping) (Kennedy et al. 1990b). They concluded that
these indicated different physiological systems that have been targeted and, therefore, could be useful in studying the underlying physiological bases of these
symptoms. They also concluded that it helped to identify the ways in which a
simulator might be causing problems for users, in terms of rectifying motion or
picture problems.
As Kennedy et al. (1991) have opined, there seemed to be a general assumption
that as simulators became more realistic, the result would yield both faster and more
efficient training. Despite this move to provide more realistic and higher quality
simulation, there didn’t appear to be a parallel improvement in training. They
believed that striving to improve realism might in fact have increased the incidence
of motion sickness. I suggest that perhaps total asynchrony is not as provocative as
simulation closer to the real world. It may be that until simulation becomes totally
synchronous, the problem will indeed get worse, as Money suggested (Money
1991).
In summary, simulator sickness clearly includes a significant element of what we
recognise to be motion sickness. In addition, there is also an element of visual
20
1 Motion Sickness
discomfort caused by the optical stimulation. Finally, there are the additional stress
and fatigue factors that Money has described as being commonly associated with
the test situation in simulator training. It is also important to reiterate the point about
creating simulator sickness by suggestion. We know that heightened arousal on
entering a provocative motion environment plays a large part in determining how an
individual will respond to that experience. So, we should be very careful in how we
present and use the numerous useful and well-meaning suggestions for minimizing
the provocative elements that may cause simulator sickness.
1.5
Performance Degradation and Effect of Severity
and Motion Sickness
In 1943 Schwab carried out an experiment on 115 naval personnel whose chronic
seasickness required treatment in hospital where they were identified as Type 1 and
Type II according to the severity of their previous motion sickness. That included
the degree of impairment of their official duties as well as their symptoms. Schwab
was able to establish that the Type I sailors were so severely upset by their seasickness that they were unable to work on board ship. On the other hand, Type II
sailors were not severely affected and were able to carry out their official duties at a
reduced level of efficiency. Shwab was very intrigued by the interaction between
those with chronic seasickness and the type of vessel they were on and so he
estimated that these Type II sailors could work at 90% of their shore efficiency on
large vessels, 60% on medium vessels and about 40% efficiency on small ships.
Whereas the Type I sailors were only able to work at 40% of their land efficiency
even on the large class of ships and only on medium ships at 5 and 10% on small
ships; but unfortunately he didn’t give any details as to how he arrived at these
particular percentages.
Birren (1949) pointed out that every study concerned with motion sickness faced
the problem of judging when a person was motion sick. Consequently, he suggested
that we should use a rating system to quantify the severity of motion sickness, see
Table 1.6.
In Chap. 13, when we were discussing our recent experiments to evaluate the
key components of cognitive-behavioural training, the severity of motion sickness
has always been limited to the subject’s threshold of response to provocative
motion. This is equivalent to the onset of Birren’s rating level 1. It is important to
Table 1.6 Birren’s ratings of
motion sickness severity
Motion sickness symptoms
Level
No symptoms
Slight nausea or other minor complaints
Nausea and sweating
Vomiting, but able to work
Incapacitated
0
1
2
3
4
1.5 Performance Degradation and Effect of Severity and Motion Sickness
21
notice that in addition to symptomatology, Birren has introduced the idea of performance degradation in his classifications. In my Royal Air Force (RAF) studies
(1974, 1965), the severity of a trainee’s motion sickness had been rated according to
its effect on his ability to absorb instructions and on his performance in flight,
irrespective of the particular symptoms. I believe strongly that adverse effects on
training or operational effectiveness are the key issues. Birren’s rating level 3 is a
very interesting one, because vomiting per se would not be reliable; many people
vomit but carry on working, whereas others give up working but don’t vomit. I had
a very good example of this in WW II, when my navigator on Wellington bombers
vomited on every trip, irrespective of the motion of the aircraft or the amount of
enemy firing.
In a military or commercial situation, where individuals are performing skilled,
critical or potentially dangerous tasks in a provocative motion environment, the
greatest threat imposed by motion sickness is the resultant degradation of performance. Birren (1949) has concluded that most people who experience a transient
bout of motion sickness can exert themselves sufficiently to perform adequately
when necessary; he called that “peak efficiency”. This need not be closely related to
the performance of the individual’s normal daily routine, which he called “maintenance efficiency.” When we were carrying out experiments on our ship motion
simulator, we found a similar situation. Birren’s assessment of the effect
provocative motion has on human performance is still relevant to today’s
warfighters.
In Birren’s words:
Even though seasick, a man may be able to exert himself to emergency performance; the
result of his efforts depends to a significant extent upon how well he has maintained his
“gear”. During rough weather, seasick personnel lose interest in doing anything except the
barest necessities, and an obvious lack of spontaneity can be observed aboard ship even in
those men who are not frankly seasick. Not only do the men fail to indulge in the usual
“horse play” and spend almost all time off-watch in their bunks, but they also fail to secure
gear properly. Such effects of seasickness upon “maintenance efficiency” should be seriously considered as having a significant effect upon personal efficiency or performance.
Colwell (1989) has described four classes of human performance degradation
associated with the motion of a ship, namely: motion sickness, motion-induced
fatigue (MIF), motion-induced interruptions (MII), and whole body vibration. Of
these, the first three are “low frequency phenomena,” which all vessels can expect
to experience much, if not most, of the time at sea. One should be a little careful
with that kind of generalisation, however; although it is true that motion sickness is
associated with a low frequency of 0.2 Hz, it requires an associated medium level
of acceleration. On the other hand, vibration is of a higher frequency. These
responses also differ from each other in terms of the result of duration of exposure.
Motion sickness alone may exhibit a reduction due to adaptation over time, whereas
all of the others cause an increase in degradation of performance with increasing
exposure.
Colwell (2000) has reported on an interesting questionnaire study at sea that
involved seven NATO frigates during two weeks of combat training exercises
22
1 Motion Sickness
during heavy winter weather in the North Atlantic Ocean. The NATO Fatigue, Sea
Sickness and Human Performance Assessment Questionnaire (PAQ) was developed by the Canadian Defence Research Establishment Atlantic to obtain a large
database on the potential adverse effects of fatigue, motion sickness and task performance caused by ship motions.
Colwell reported that problems associated with sleep quality and fatigue have
shown consistently high severity levels across the database. He pointed out that
since high fatigue responses in turn correlate significantly with a number of cognitive performance problems this has constituted a serious problem in terms of
performance degradation. Reports of difficulties associated with motion sickness
have shown a lower severity. On the other hand they have demonstrated a high
correlation with problems associated with both cognitive and physical tasks, particularly involving task abandonment. He pointed out that low to moderate levels of
motion sickness have serious consequences in terms of a warfighter’s operational
efficiency.
1.6
Sopite Syndrome
The sopite syndrome is said to be a response to provocative motion that, as the
name suggests, is characterized by drowsiness and mental depression. Other
symptoms include fatigue, difficulty in concentrating and disturbed sleep. As previously stated, Graybiel and Knepton (1976), unlike many of their predecessors in
the field of motion sickness, have reported that drowsiness is one of the cardinal
symptoms of motion sickness. Apart from the presence of such responses among
other major symptoms and signs of motion sickness, they noted that this syndrome
may be found in the absence of these other features or after they have disappeared.
This led them to believe that these symptoms of the sopite syndrome may have a
different time course from the other major features of motion sickness. They have
concluded that the relatively slow disappearance of these symptoms indicated the
presence of a neuro-humoral causative factor.
It has also been noted by Benson (1988) that sleepiness is a symptom which is
commonly experienced by those exposed to unfamiliar provocative motion even if
the individuals have not reported other typical motion sickness responses. In our
laboratory, we have recently noted that subjects have frequently reported drowsiness when exposed to provocative motion in our ship motion simulator. However,
as we shall see later in this section, this response might not necessarily have been
the result of the motion. As long ago as 1912, Byrne had referred to the effects of
seasickness on the nervous system and stated: “The psychic depression is frequently
so extreme and cerebral function so completely perverted that self-control becomes
an impossibility.” In 1936, Hill reported that sleep had an important bearing on
seasickness, pointing out that drowsiness, apathy and mental lethargy, without
somnolence, were present.
1.6 Sopite Syndrome
23
Lawson and Mead (1998), whilst indicating that this syndrome has been little
understood, nevertheless have suggested that it is a distinct syndrome from either
what we know as motion sickness or a state of fatigue. They also considered that it
could have particularly profound effects in situations where, for other reasons, sleep
disturbances already existed in different transport environments. Sleep disturbances
are very common at sea, and this may mask the sopite syndrome, if indeed it is a
separate entity. Whether that is the case or not, sleepiness and fatigue have been
commonly reported in provocative motion environments. Lawson and Mead
stressed that the sopite syndrome did appear to have a different time course from the
other symptoms of motion sickness; that it commonly appeared before nausea, and
persisted after the nausea had disappeared. Reverting to experiences in our laboratory, we have noticed significant yawning and apparent sleepiness both before the
onset of nausea and after the end of provocative motion. Also, there have been
reports of nausea during the follow-up period after these events have taken place.
Lawson and Mead have raised an important issue, namely that even mild sopite
syndrome responses could create a significant problem if they were not readily
recognised. Certainly, it has been our experience at NBDL that general discomfort
is a common symptom of motion sickness and this may be related to the sopite
syndrome if indeed that syndrome is associated more directly with low-grade
motion sickness. They have also provided a number of anecdotal reports concerning
the sopite syndrome. These are very interesting because they cover a wide range of
situations. In one case, during a low-level navigation sortie in bumpy conditions, an
observer had noticed that a student passenger in the aircraft had fallen
asleep. However, in that situation, it is quite likely that the aircraft motion had been
sufficiently provocative as to cause conventional motion sickness responses. At the
other end of the spectrum, they have reported individuals being sleepy when driving
on long road trips in conditions that, presumably, were not particularly provocative.
In another situation, a flight surgeon has reported crewmembers becoming extremely drowsy and suffering mood depression during rough seas. They have
described tank crews reporting drowsiness during the movement of the vehicle and
also subsequently, after the vehicle had stopped for a rest break. A former SkyLab
astronaut has reported sluggishness and loss of appetite, which he attributed to what
he has called “sub-clinical motion sickness.”
In that same year (1998) Flaherty et al. performed a thesis entitled “Sopite
Syndrome in Operational Flight Training” stating that the sopite syndrome was a
response to motion typified by drowsiness. fatigue, disturbances of sleep and
changes of one’s mood. They began by reviewing various research papers on the
sopite syndrome that had already been published by: Graybiel and Knepton (1976),
Lawson and Mead (1997) and Askins et al. (1997). They felt that these papers had
often gone unrecognised because they were not a part of the symptomatology that
was associated with what they called “regular” motion sickness. To that point,
(Lawson and Mead 1997) were of the opinion that “Sopite Syndrome” was not
correctly associated with the motion that incites its arousal. In their opinion it was
different from ordinary motion sickness or common or garden fatigue and what is
more, it might seriously affect both motor vehicle drivers and aircraft operators
24
1 Motion Sickness
Although they felt that the sopite syndrome might have an effect on these people,
but if so, it was it was relatively unknown. As a result they decided to join the effort
that was being undertaken to investigate the incidence, seriousness and significance
of the sopite syndrome on student naval flight officers.
In 1991, Guedry wrote a Chapter entitled “Motion Sickness and its Relation to
Some Forms of Spacial Orientation: Mechanisms and Theory” in AGARD Lecture
Series 175, published September 1991. In a sub-para entitled Frequency-Effects and
Stott’s Utricle-Saccule Rule, he wrote: “the utricle-saccule rule, used to explain
sickness induced by vertical linear acceleration, appeals to the fact that frequencies
of linear oscillation that induce sickness are considerably below those normally
encountered in locomotion activity so that, for example, the mean 1 g intensity rule
would be violated on the high side for almost 2 s and then on the low side for
almost 2 s in each cycle of a 0.25 Hz vertical linear oscillation. This interesting
explanation leads to one of the more perplexing facts of motion sickness that must
be dealt with by any comprehensive model of motion sickness. Motion sickness is
dependent on the frequency of motion stimuli, for some and perhaps all forms of
sickness producing motion stimuli.”
Data that are available have suggested that 0.2 Hz frequency are maximally
provocative (Guignard and McCauley 1990; Hanlon and McCauley 1974) and that
higher and lower frequencies are are less provocative if the acceleration levels given
are peak vertical. Since frequencies that are above 0.5 Hz are less provocative
demonstrates that the utricle and saccule are stimulated during walking and running
if the frequencies are above 1 Hz. If the low frequencies are appreciably below
0.2 Hz Stott’s 1 g explanation wouldn’t be valid. Low frequency data of vertical
oscillation are weak, because they need great linear displacement needed to reach
the peak acceleration levels at 0.2 Hz. As Lawther and Griffen pointed out in 1986,
magnitude as well as frequency is important. If amplitudes are needed at very low
frequencies, they are greater than those that can be reached with the existing motion
equipment.
Lawther and Griffen (1986) reported on a study from 17 voyages on one particular vessel in which the sea ratings ranged from calm to very rough, during which
the vertical motion on board was less than 0.1 m s−2 r.m.s. to nearly 1.0 m s−2 and
the incidence of vomiting ranged from 0% to nearly 40%; there was a high correlation between the z-axis motion of the ship and both the incidence of vomiting
and the illness rating. Although a large number of the passengers on board who felt
unwell didn’t vomit, there was a significant correlation between the incidence of
vomiting and the illness rating; the mean illness rating increased with the duration
at sea and the number who vomited also increased with the duration of the trip.
A similar data analysis from other trips on that line was reported by these authors
in 1988. From the questionnaires that were obtained from the author’s reported that
from these studies, that overall 7.0% of passengers vomited at some time on their
voyage, 21.3% felt “slightly unwell”, 4.3% felt “quite Ill” and 4.1% felt “absolutely
dreadful” Vomiting incidence and illness ratings were highest in females (a male to
female ratio of 3–5) and there was a slight reduction in sensitivity with increasing
age (mostly due to an increase below 15 years). The incidence of vomiting and
1.6 Sopite Syndrome
25
illness ratings were both greater in those passengers who had the least experience of
travel at sea. Twice as many of those passengers vomited in that group which was
taking anti-motion sickness drugs compared with the group that was not taking any
drugs. That effect was probably due to a greater use of drugs in that group who were
more susceptible to motion sickness. The consumption of alcohol during these
voyages was also associated with a lower incidence of vomiting and illness; that
was probably due to the fact that those who were prone to sickness were less likely
to consume alcohol when exposed to motion.
Matsangas and McCauley (2014) have written “The Effect of Mild Motion
Sickness and Sopite Syndrome on Multitaxing Cognitive Performance”. In their
introduction, they began by summarising their views on motion sickness in healthy
individuals as a: “common syndrome that occurs when people are exposed to real or
apparent motion with which they are unadapted”.
For example, they refer to the variety of signs and symptoms of the condition
that have been well described by Benson (2002). They also refer to Graybiel and
Knepton who referred to the “Sopite Syndrome” in 1976 and this will be discussed
later. As they point out, depending on the susceptibility of the person involved with
a particular event and the characteristics of the motion involved, this particular
sopite syndrome may be the only particular manifestation of a sample of motion
sickness (Graybiel and Knepton 1976; Mead and Lawson 1997).
Various accounts and reports over the last hundred years have suggested that
even those who are sick can continue to work successfully if they are highly
motivated (Baker 1966) and if successfully encouraged to suppress symptoms, it
increases one’s tolerance (Dobie and May 1994). We were unable to identify any
particular studies that explored the effects of motion sickness, obtaining learning/
skill and reminiscence, that is to say, the improvement of performance of any
partially learned task in the absence of specific practice (Eysenck and Frith 1977,
p. 3).
Given these gaps in research. This work focused on this somewhat gray area of
mild motion sickness, where some symptoms do exist but the severity of the
malaise is low. Here we have the phrase mild motion sickness used to describe
symptoms related to motion sickness that do not incapacitate; the person is not
feeling moderate or serious malaise and continues to carry out the given task. This
study that is assessed in controlled conditions the very hypothesis that multitasking
has been significantly reduced by mild motion sickness and soporific effects.
In their analytical plan, the statistical equivalence between the three participant
groups was assessed, including age, gender, height weight, MSQ ratings and the
time of day that each experimental session was started. They then assessed the
effect of motion sickness on performance. Within each of the motion sessions, two
analyses were used. In the first, a correlational analysis was carried out between the
average performance scores for each volunteer, with the corresponding motion
sickness severity average. In the second group a comparison of performance scores
was carried out between the symptomatic and asymptomatic volunteers. These two
groups had been chosen in order to compare each average symptom severity for
both the motion and static conditions. If motion symptom severity was greater than
26
1 Motion Sickness
the static, the volunteer was classified as “symptomatic” If less or equal to the static
condition, the volunteer was considered “neutral”.
Their research results showed that performing cognitive multitasking declined
even if both motion sickness and soporific symptoms were mild. The performance
differences in the composite scores (9.43%), as well as in the memory (31.7%) and
arithmetic task scores (14.7%) between “symptomatic” and “asymptomatic” were
significant but only in the second session. So, during the first motion session, the
volunteers seem to overcome mild motion sickness but in the second motion session, the symptoms of motion sickness take a toll on performance.
The results also suggest that mild motion sickness doesn’t interfere with the
retention of a performance in a cognitive multitasking environment. The pattern of
retention of performance between the two sessions was not associated with the
existence of the stimulus of motion or the development of the symptoms of mild
motion sickness in the first session. It is possible that this may have been due to the
level at which mild motion sickness interferes with cognitive performance in the
first session, that is when the volunteers are still novices. It is reasonable to suggest
that novice participants will overcome the detrimental effects of mild motion
sickness by focusing more on the multiple tasks during that first session since the
tasks will seem to be more novel and interesting.
1.7
A Sopite Syndrome Thesis
A thesis entitled “Sopite Syndrome on Operational Flight Training” was carried out
by Flaherty, Schmit, Read and Buttrey ast the Naval Postgraduate school in 1998.
They began by reviewing various research papers on the sopite syndrome that had
already been published by: Graybiel and Knepton (1976), Lawson and Mead
(1997), Askins et al. (1997) and Lawson and Mead (1997). They felt that these
papers had often gone unrecognized because they were not a part of the symptomatology that was associated with what they called “regular” motion sickness. To
that point, Lawson and Mead (1997) were of the opinion that to that degree; “Sopite
Syndrome was not correctly associated with the motion that incites its arousal”.
The symptoms of the Sopite Syndrome were usually merged with those associated with: “regular” motion sickness, but as Lawson and Mead (1997) pointed
out, there were two particular cases in which the Sopite Syndrome was alone for
these particular symptoms. One was when the size of the elicitating stimuli was at
or near an individual’s susceptibility; the other took place during a lengthy exposure
in a situation where a person adapts to the environment, resulting in the sudden or
gradual disappearance of the symptoms of motion sickness symptoms apart from
reactions that were like those of the Sopite Syndrome. So, Lawson and Mead in
1997 are of the opinion that, on occasion, the only sign of motion sickness are the
symptoms of Sopite Syndrome; these have been called “pure Sopite Syndrome”;
these can last long after nausea and vomiting and be quite debilitating. So, apart
from the difference of symptoms, Sopite Syndrome seems to occur at different times
1.7 A Sopite Syndrome Thesis
27
in terms of the development and persistence of motion sickness. It was in 1976
when Graybiel and Knepton decided that the time course of the Sopite Syndrome
was different from the general symptoms of “regular: motion sickness”.
It has been found that a lengthy exposure in a rotating device is uncommon in
many important ways from what an individual would feel in high seas or dynamic
flight (Lawson and Mead 1997). For example, in a rotating environment the subject’s movements are needed to start the unusall accelerations, whereas, at sea or in
flight, fixing the head and body might relieve the effects but wouldn’t stop the
unusual external forces that the subject experiences (Graybiel et al. 1965). So, when
a subject is seated in a slow rotating room with head fixed or sleeping, the experience is not very different from a stationary room. Movements that cause interference seem to fall into two categories; whole body movements and the rotation of
the head out of the plane of rotation of the room.
It is possible that Sopite Syndrome acts upon some other medical illnesses. As
an example, in a case of chronic depression, it has been reported that a 27 year old
aviator described himself as being depressed and that it had been some two years
since he last felt happy (Moore and McDonald 1993). Apparently ha lacked
motivation, had trouble and complained of experiencing “blank stares” and lsack of
attention to detail. He also said that he often woke up very early and withdrew from
others, including his wife, and avoided making any social contact, if possible.
Apparently, the state of depression began with his joining the United States Navy in
the aviation field. So, is possible that the Sopite Syndrome might have either
interacted with or confused the diagnosis of chronic depression he had been given.
Sopite Syndrome is nearly always present in airsickness; similarly it is found in
other types of motion sickness, such as sea or airsickness (Graybiel and Knepton
1976). Current research seems to suggest that a small number of student aviators
describe symptoms that suggest the syndrome even after a very short time. As a
result, in some cases, it has been suggested that Sopite Syndrome is a potential
hazard. The main components of drowsiness, fatigue, sleep disturbancies and mood
shifts are a concern since a short time of one’s attention could be dangerous on
board some form of transport. Furthermore; a merthodicsal plan is needed to decide
to what extent these kinds of deficits are actually attributed to Sopite Syndrome.
In a recent study at our laboratory at NBDL, we examined the development of
the sopite syndrome responses under different conditions of motion, sensory
stimulation and mental workload. The two motion profiles that were used simulated
a smaller class of ship (frigate) with a typically large motion profile and an aircraft
carrier with provocative motion primarily in pitch and roll and very much less
heave than the frigate. We also used a static (control) condition; that was an
important feature that was lacking in previous observations by others. In the first
part of the experiment we attempted to compare the motion sickness responses of
the two categories of ship and a static control condition. Significant trial effects
were obtained for only four symptoms; drowsiness, boredom, stomach awareness
and fullness of the head. These results suggested that these particular symptoms
were not related to motion, per se, and have been associated with the burning
question regarding whether the sopite syndrome is motion induced or simply due to
28
1 Motion Sickness
inactivity. The effects of mental workload in a later part of the study may have
reduced motion sickness and sopite responses. In this study, that issue was not
clear-cut because the repeated exposure to provocative motion might have induced
adaptation. As a result further investigation is certainly needed to clarify the cause
of these symptoms of the sopite syndrome. They may simply be typical symptoms
of low-grade motion sickness occurring during and or after exposure to provocative
motion. However, they may also be associated with straightforward environmental
factors such as high ambient temperature, isolation or exposure to enclosed spaces.
Until all of these possibilities are investigated further, in a controlled fashion, this
question of the sopite syndrome being part of motion sickness or merely a separate
entity remained open.
1.8
Motion Sickness as a Stressor
To continue, considering that motion sickness is a stressor, the researchers felt that
their findings might be due to a perspective of performance under stress. The
deterioration of task performance in cognitive tasks (memory and arithmetic) is in
agreement with stress research (van Hiel and Mervielde 2007). Simple tasks that
need automated responses will suffer less from stress than, for example, complex
tasks underlying cognitive control. So, why do we see this deleterious effect of
motion sickness on cognitive performance? Is it due to keenness or perhaps the lack
of it or due to changes in the capacity of resources, such as limitations of working
memory? These results seem reasonable also from the point of view of a perspective of attentional capacity overload (Matthews and Desmond 1995). The
arithmetic task was the worst, followed by the short-term memory. The visual and
auditory tasks did not seem to be affected at all. This particular hierarchy is consistent with the multiple resource theory (Wickens 2002; Wickens and Hollands
2000) which suggests that the sensory processing of the peripheral visual and
auditory systems is relatively resource-free (Wickens and Hollands 2000). In that
case, the reduction of access to attentional resources due to motion sickness will
only have a small effect on the visual and auditory tasks. These results suggest that
motion sickness acts like a distraction or diversion and so. difficulties in focused
attention should be among the major symptoms in mild motion sickness. It has
already been stated, however, that researchers have also identified that involvement
with a mental task may decrease motion sickness (Bos 2011). The inverse relationship between the severity of motion sickness and cognitive effort might be
explained from a cognitive resources and cognition control perspective.
In addition, I saw motion sickness as a stressor when I was working on my
cognitive-behavioral training programme. The advisor focuses on the psychological
aspects of stress management and endeavours to instill a belief the individual can
indeed tolerate noxious or stressful situations. Once this idea has been established,
it is reinforced by means of controlled exposures to non-specific provocative
motion stimuli.
1.9 Summary
1.9
29
Summary
• Motion sickness constitutes maladaptation to a novel inertial environment.
• Motion sickness is exhibited by a person showing physical signs and symptoms
of a bodily disturbance. These are a result of a built-in protective response
caused by exposure to provocative motion environments for a sufficient length
of time.
• The main symptom of motion sickness is nausea. The main signs are pallor,
sweating and vomiting. Other responses include apathy, general discomfort,
headache, stomach awareness, increased salivation, prostration, drowsiness and
hyperventilation.
• Drowsiness and mental depression are part of a symptom-complex called the
sopite syndrome. Other symptoms include fatigue, difficulty in concentrating
and disturbed sleep. It is still unclear if the sopite syndrome is related to motion
sickness.
• Performance degradation is of the utmost importance when dealing with human
operators and the effects that motion sickness may have on their ability to
perform tasks effectively.
References
Ambrose SE (1944) The climactic battle of world war II. Simon and Schuster, New York, NY
Askins K, Mead AM, Lawson BD, Bratley MC (1997) Sopite syndrome study I: Isolated sopite
symptoms detected post hoc from a preliminary open-ended survey of subjective responses to a
short-duration visual-vestibular stimulus. Abstracts of the Aerospace Medical Association 68th
Annual Scientific Meeting, p. 204
Bacon G (1915) Flying in peace and war (Chap. VI). In: All about flying. Methuen’s sport series.
Methuen & Co. Ltd., London, p 102
Baker CH (1966) Motion and human performance: A review of the literature (Tech.
Rep. No. 770-1 Section I). Goleta, CA: Human Factors Research
Bayliss M (1940) Studies of the mechanism of vomiting produced by staphylococcus enterotoxin.
J Exp Med 72:669–684
Benson AJ (1988) Motion sickness. In: Ernsting J, King P (eds) Aviation medicine, 2nd ed.
Butterworth-Heinemann Ltd., Oxford
Benson AJ (2002) Motion sickness. In: Pandoff KB & Burr RE (eds) Medical aspects of harsh
environments, Washington, DC: U.S. Army Medical Department, Borden Institute, 2:1048–
1083
Birren JE (1949) Motion sickness: its psychophysiological aspects. A survey report on human
factors in undersea warfare. Committee on Undersea Warfare, National Research Council,
Washington, D.C. pp 375–398
Bos JE (2011) Less sickness with more motion and related issues (Final Report No. TNO-DV
2011 A154). Soesterberg, Netherlands: TNO, Behavioural and Societal Sciences
Byrne J (1912) On the physiology of the semicircular canals and their relation to seasickness. J. T.
Dougherty, New York
30
1 Motion Sickness
Casali JG (1986) Vehicular simulation-induced sickness. An overview, vol 1. NTSC-TR-86-010,
Naval Training Systems Center, Orlando, FL
Chipriani A, Morton G (1942) Studies of blood pressure, electrocardiograms, and respiratory
tracings in volunteers. In: Of the conference on motion sickness. National Research Council of
Canada Rept. No. C744
Colwell JL (1989) Human factors in the naval environment: a review of motion sickness and
biodynamical problems. Canadian National Defence, DREA Technical Memorandum 89/220
Colwell JL (2000) NATO questionnaire: correlation between ship motions, fatigue, sea sickness
and Naval task performance. In: Trans RINA conference on human factors in ship design and
operation, September, London
Crampton GH (1955) Studies of motion sickness: XVII. Physiological changes accompanying
sickness in man. J Appl Physiol 7:501
Davis D, Goode EU, Weiss S (1932) Localization of afferent visceral impulses in spinal cord. Arch
Intern Med 470–479
De Zouche I (1894) In: Quain’s, a dictionary of medicine, vol II, 2nd edn
DePuy WH (1896) Sea-sickness. In: The encyclopædia Britannica, a dictionary of arts, sciences,
and general literature, vol XXI. The Werner Company, MDCCCXCVI, Chicago
Dichgans J, Brandt T (1973) Optokinetic motion sickness as pseudo-Coriolis effects induced by
moving visual stimuli. Acta Otolaryngol 76:339–348
Dobie TG (1989) Teaching the right stuff—the heart of the matter. Aviat Space Environ Med
60:195–196
Dobie TG, May JG (1994) Cognitive-behavioral management of motion sickness, vol 65, pp C1–
C20 (monograph)
Eysenck HJ, Frith CD (1977) Reminiscence, motivation and personality. New York: Plenum
Flaherty DE (1998) Sopite syndrome in operational flight training. Naval Postgraduate School,
Master's thesis, Monterey, CA
Frank L, Kennedy RS, McCauley ME, Kellog RS (1983) Simulator sickness: a reaction to a
transformed perceptual world, I. scope of the problem. In: Proceedings of the second
symposium of aviation psychology. Aviation Psychology Laboratory, Ohio State University,
Columbus Ohio
Gay LN (1954) Labyrinthine factors in motion sickness. Int Rec Med General Pract Clin 176
(12):628–630
Gellhorn E, Loofbourrow GN (1963) Emotions and emotional disorders. A neurophysiological
study. Harper & Row, New York, NY
Gillingham KK (1966) A primer of vestibular function, spatial orientation, and motion sickness.
Review 4–66 (U. S. Air Force School of Aerospace Medicine, Brooks AFB, TX)
Glaser EM (1959) Prevention and treatment of motion sickness. Proc Royal Soc Med London
52:965–972
Golding JF (1992) Phasic skin conductance activity and motion sickness. Aviat Space Environ
Med 63:165–171
Graybiel A, Knepton J (1976) Sopite syndrome: a sometimes sole manifestation of motion
sickness. Aviat Space Environ Med 47:873
Graybiel A, Kennedy RS, Knoblock EC, Guedry FE, Hertz W, McCleod M, Colehour JK,
Miller EF, Fregly A (1965) Effects of exposure to a rotating environment (10 RPM) on four
aviators for a period of twelve days. Aerosp Med 36:733–754
Guedry FE (1991) Motion sickness and its relation to some forms of spatial orientation:
mechanisms and theory. Motion sickness: significance in aerospace operations and prophylaxis, AGARD lecture series 175 (AGARD-LS-175), North Atlantic Treaty Organization
Advisory Group for Aerospace Research and Development, Neuilly-sur-Seine, France, vol 2,
p1
Guignard JC, McCauley ME (1990) The accelerative stimulus for motion sickness; In: GH
Crampton (ed) Motion and space sickness, Boca Raton, FL: CRC Press, pp 123–152
Hallion RP (2003) Taking flight. Oxford University Press, New York, NY
References
31
Harm DL (1990) Physiology of motion sickness symptoms. In: Crampton GH (ed) Motion and
space sickness. CRC Press Inc., Boca Raton, FL
Hatcher RA, Weiss S (1922) The seat of emetic action of the digitalis bodies. Arch Intern Med
29:690–704
Hemingway A (1944) Cold sweating in motion sickness. Am J Physiol 141:172–175
Hill J (1936) The care of the sea-sick. Br Med J II:802–807
Homick JL, Reschke MF, Vanderploeg JM (1984) Space adaptation syndrome: incidence and
operational implications for the space transportation system program. In: Motion sickness:
mechanisms, prediction, prevention and treatment. In: AGARD conference proceedings no.
372, North Atlantic Treaty Organization Advisory Group for Aerospace Research and
Development, Neuilly-sur-Seine, France, vol 36, pp 1–6
Irwin JA (1881) The pathology of sea-sickness. Lancet, II:907–909
Isu N, Koo J, Takahashi N (1987) Changes of skin potential level and of skin resistance level
corresponding to lasting motion discomfort. Aviat Space Environ Med 58:136–142
Jasper HH, Morton G (1942) Electroencephalography in relation to motion sickness in volunteers.
In: Proceeding of the conference on motion sickness. National Research Council of Canada,
Report No. C745
Kennedy RS, Frank LH (1984) A review of motion sickness with special reference to simulator
sickness. Prepared for distribution at the National Academy of Sciences/National Research
Council Committee on human factors workshop on simulator sickness; 26–28 September,
1983, Naval Postgraduate School, Monterey, CA (Revised 9 March 1984.)
Kennedy RS, Dunlap WP, Fowlkes JE (1990a) Prediction of motion sickness susceptibility. In:
Crampton GH (ed) Motion and space sickness. CRC Press Inc., Boca Raton, FL, pp 179–215
Kennedy RS, Hettinger LJ, Lilienthal MG (1990b) Simulator sickness. In: Crampton GH
(ed) Motion and space sickness. CRC Press, Inc., Boca Raton, FL, pp 317–341
Kennedy RS, Smith MS, Jones SA (1991) Variables affecting simulator sickness: report of a
semi-automatic scoring system. In: Proceedings of the sixth international symposium on
aviation psychology, Columbus, OH
Kennedy RS, Lane NE, Berbaum KS, Lilienthal MG (1993) A simulator sickness questionnaire
(SSQ): a new method for quantifying simulator sickness. Int J Aviation Psychol 3(3):203–220
Lackner JR, Graybiel A (1980) Evaluation of the relationship between motion sickness
symptomatology and blood pressure, heart rate, and body temperature. Aviat Space Environ
Med 51:211–214
Lackner JR, Graybiel A (1986) Sudden emesis following parabolic flight maneuvers: implications
for space motion sickness. Aviat Space Environ Med 57:343–347
Lawson BD, Mead AM (1997) The sopite syndrome revisited: drowsiness and mood changes
during real or apparent motion, Paper presented at the 12th Annual Man in Space Symposium,
“The Future of Humans in Space,” Washington, D.C.
Lawson BD, Mead AM (1998) The sopite syndrome revisited: drowsiness and mood changes
during real or apparent motion. Acta Astronaut 43(36):181–192
Lawther A, Griffin MJ (1986) The motion of a ship at sea and the consequent motion sickness
amongst passengers. Ergonomics 29(4):535–552
Lindsley DB, Wendt GR (1944) Investigation into the relationships of EEG to motion sickness
susceptibility. Division of Anthropology and Psychology, National Research Council,
Appendix B
Llano GA (1955) Airmen against the sea: an analysis of sea survival experiences. ADTIC
Publication G-104, Montgomery, AL; Research Studies Institute, Maxwell Air Force Base
Lynn R (1966) Attention, arousal and the orientation reaction. Pergamon Press, Oxford
Marti-Ibanez F (1954) Philosophical perspectives of motion sickness. Int Rec Med General Pract
Clin 176(12):621–626
Matsangas P, McCauley ME, Becker W (2014) The effect of mild motion sickness and sopite
syndrome on multitasking cognitive performance. Hum Factors, 56(6):1124–1135
Matthews G, Desmond PA (1995) Stress as a factor in the design of in-car driving enhancement
systems. Le Travail Humain 58:109–129
32
1 Motion Sickness
McClure JA, Fregly AR, Molina E, Graybiel A (1971) Response from arousal and thermal sweat
areas during motion sickness. Report NAMRL-1142, Naval Aerospace Medical Research
Laboratory, Pensacola, FL
McEachern D, Morton G, Lehman P (1942) Seasickness and other forms of motion sickness. 1.
General review of the literature. War Med 2(5):410
Mead AM, Lawson BD (1997) Sopite syndrome case report I: Motion-induced drowsiness and
mood changes in an individual with no other motion sickness symptoms. A case of “pure”
sopite syndrome? Aviat Space Environ Med 68(3):648
Money KE (1970) Motion sickness. Physiol Rev 50:1–38
Money KE (1991) Simulator sickness. In: Motion sickness: significance in aerospace operations
and prophylaxis. AGARD-LS-175. NATO/AGARD, Neuilly-sur-Seine, 6B, 1–4
Moore JL, McDonald WA (1993) A case of chronic depression, Aviat Space Environ Med
pp 1051–1054
Morton G, Cipriani A, McEachern D (1947) Mechanism of motion sickness. Arch Neurol Psych
57:58–70
Nicogossian AE, Parker JF (1982) Space physiology and medicine. NASA SP-447. NASA
Scientific and Technical Branch
O’Hanlon JF, McCauley ME (1974) Motion sickness incidence as a function of the frequency of
acceleration of vertical sinusoidal motion. Aerosp Med 45(4):366–369
Reason JT, Brand JJ (1975) Motion sickness. Academic Press, New York, NY
Schwab RS (1943) Chronic seasickness. Am Int Med 19:28–35
Steele JE (1968) The symptomatology of motion sickness. NASA SP-187. In: Fourth symposium
on the role of the vestibular organs in space exploration. Naval Aerospace Medical Institute,
Pensacola, Florida
Treisman M (1977) Motion sickness: an evolutionary hypothesis. Science 197:493–495
Turner M, Griffin MJ (1995) Motion sickness incidence during a round-the-world yacht race.
Aviat Space Environ Med 66:849–856
Tyler DB, Bard P (1949) Motion sickness. Physiol Rev 311–369
van Hiel A, Mervielde I (2007) The search for complex problem-solving strategies in the presence
of stressors, Hum Factors, 49:1072–1082
Warwick-Evans LA, Church RE, Hancock C, Jochim D, Morris PH, Ward F (1987) Electrodermal
activity as an index of motion sickness. Aviat Space Environ Med 58:417–423
Wickens CD (2002) Multiple resources and performance prediction. Theoretical Issues in
Ergonomics Science, 3:159–177
Wickens CD, Hollands J (2002) Engineering psychology and human performance, 3rd edn. Upper
Saddle River, NJ: Prentice Hall
Chapter 2
Incidence of Motion Sickness
Abstract Now that we have a basic understanding of what the term “motion
sickness” means and how it affects the individual, we can examine the problem in
more detail. We shall begin by getting a feel for just how common motion sickness
has been found to occur in various forms of provocative motion. I am sure that these
numbers will convince you that this response is prevalent across the population.
This in itself would support what I said in the last chapter, namely, that this is a
perfectly normal protective response and we should not be surprised at the high
incidence that is associated with the various modes of transport. It should also alert
us to the fact that motion sickness can have a significant effect on crew performance
and operational efficiency. Although I seem to stress the military situation, one must
not forget that this malady is also equally common in both commercial and social
settings.
Motion sickness is certainly very common. From their early exposure to
provocative motion, however, people vary in their response. I believe that these
early experiences can be critical in determining if an individual is likely to adapt to
these provocative motion stimuli or become sensitised. In the latter case, individuals
slowly but surely come to believe that unlike others, they are particularly sensitive
to motion and thereby lapse into becoming chronic motion sickness sufferers. In
addition, many other species are susceptible to this malady. For example the susceptibility of dogs is similar to man, whereas horses, cows, monkeys, chimpanzees,
seals and some birds are somewhat less so (Money and Myles 1975). These authors
have also pointed out that certain species of fish can become seasick when conveyed in a tank on a vessel in rough seas.
The incidence of motion sickness is extremely variable depending upon the
circumstances that trigger it. Such variables as adaptation, the type of vehicle or
craft involved and the local weather conditions can all have an important effect
upon incidence. Money (1970) has reported many secondary aetiological factors
that have apparently contributed to the onset of a particular type of motion sickness.
These include vision, body position, cerebral influences, smell, exposure to
chemicals and temperature; as well as the sex and age of the individual. These
© Springer Nature Switzerland AG 2019
T. G. Dobie, Motion Sickness, Springer Series on Naval Architecture,
Marine Engineering, Shipbuilding and Shipping 6,
https://doi.org/10.1007/978-3-319-97493-4_2
33
34
2 Incidence of Motion Sickness
features will be discussed later. In addition, accurate information is not always
forthcoming and that can significantly hide the true incidence of this syndrome.
Although it has been reported that less than 5% of motion susceptible individuals
fail to adapt to provocative motion stimuli (Steele 1968), this is still a widespread
problem. Many people avoid various forms of motion stimuli in an attempt to solve
their problem because of earlier uncomfortable experiences with provocative
motion. Darwin was one such person who seemed to fail to adapt, remaining very
much susceptible to seasickness during his extended voyage on the Beagle (Barlow
1946).
As Reason and Brand (1975) have pointed out, “Any quantitative estimate of the
degree of incidence [of motion sickness] in the general population is inevitably
limited both by the method of measurement and by the sampling procedures
adopted”. For example, where motion sickness questionnaires try to obtain information from subjects about their response to a wide range of provocative motions,
the results are likely to underestimate the real figure, because of the subjects’
limited experience of different motions. In addition, there is always the question of
veracity, particularly when the answer to the questionnaire can have a significant
effect on acceptance or not for a professional appointment, see Chap. 8. Although
results based on actual exposure to provocative motion are less likely to underestimate, they tend to be specific to the particular type of condition involved. Reason
and Brand have concluded that all people with intact and functioning vestibular
systems can be made motion sick, provided that they are “given the right quality
and quantity of provocative motion.” In addition, individuals vary both widely and
consistently in their particular degree of susceptibility to motion sickness. I will
return to this matter when discussing the question of arousal in relation to motion
sickness, in Chap. 6. There are other perfectly good reasons that make it difficult to
give a precise figure for the incidence of motion sickness because a number of
factors are involved. For example:
• The characteristics of the stimulus in terms of frequency, intensity, direction and
duration. Experiments on vertical oscillators which simulate the heave component of ship motion have shown that the incidence increases as the frequency of
oscillation falls. The most provocative frequency has been shown to be around
0.2 Hz (McCauley et al. 1976; O’Hanlon and McCauley 1974).
• The susceptibility of the individual is based upon a variety of physiological
characteristics, past experiences, psychological and personality factors (Dobie
et al. 1989).
• Individual activity at the time of exposure to the stimulus, e.g., passengers are
usually worse off than drivers.
• Other factors, such as food, ambient air temperature and certain odors have also
been included.
By way of example, let us now look at the incidence of motion sickness that has
been reported for some of the different commonly experienced forms of provocative
motion; these have ranged widely and are continuing to increase.
2.1 Seasickness
2.1
35
Seasickness
Seasickness is the most common form of motion sickness. Heavy seas produce
undesirable motion responses that reduce the efficiency of crewmembers and
seriously degrade their ability to perform their operational and maintenance tasks,
either from the point of view of willingness or sheer physical impracticability. In
heavy seas, a ship is exposed to increased hull/sea resistance that is usually
aggravated by additional air resistance due to accompanying high winds. These
factors can be further aggravated by wetness when the bow ships water. In particularly heavy sea conditions slamming occurs because of the pressure that the sea
imposes on the hull of the ship. The resultant sudden changes in vertical acceleration have a seriously adverse effect on crewmembers’ abilities to maintain postural
stability and carry out their particular tasks. These problems are likely to be worse
in a littoral role, in a shallow draft situation. This calls for good seakeeping to
ensure operational efficiency. A ship’s mission capability is affected by a variety of
different factors such as type of hull design, seaworthiness, crewmember training,
readiness and adaptation to motion, on-board off-duty habitability, course heading,
varying sea state, and weather conditions. Many of these factors can be optimised in
the design cycle of the ship, ultimately, however, the operational mission may be
put at risk by unpredictable sea and wind conditions. Every activity onboard a
vessel is to some extent directly affected by the weather conditions surrounding that
vessel.
The incidence of seasickness is extremely variable. Individual responses depend
a lot on the sea conditions when individuals are first exposed to provocative motion
and how often they go to sea. If an individual’s introduction to small boats is
pleasant, reasonably frequent and in fairly calm waters, that individual is likely to
gain his or her “sea legs” and be relatively free of this malady. Similarly, people
usually get their “sea legs” after a few days at sea on an ocean voyage. Not only
does their gait become more normal, as distinct from being erratic and unsteady, but
the person is less likely to become seasick. In situations, opposite to those
described, that do not permit adaptation to take place, motion sickness is a common
occurrence. The question of adaptation to provocative motion is discussed further in
Chap. 7.
In 1964, Walters reported on a study that had been carried out in the British
Royal Navy in which medical officers indicated the number of cases of seasickness
on each day at sea, together with relevant information on the sea conditions. He
considered the figures to be conservative because they did not include those
crewmembers who had not reported sick, despite feeling ill. Nor had they included
those individuals who, aware of their susceptibility to seasickness, had taken
medication that they knew to be effective in their particular case. The study
included the crews of 5 small ships that together spent a total of 93 days at sea in
the North Atlantic during the autumn of 1963. Overall, they contributed to 8628
man/days of sea experience in weather conditions that had varied from flat calm to
full gale. Their experience with seasickness is shown in Table 2.1.
36
2 Incidence of Motion Sickness
Table 2.1 Overall loss of efficiency due to seasickness in men at sea (all weathers)
Total days
at sea
Total man/
days of
experience
Number
unaffected
(man/days)
Number affected
but not vomiting
(man/days)
Number
vomiting
(man/days)
Number
incapacitated
(man/days)
93
8628
(100%)
7449
(88.3%)
1060 (12.3%)
105 (1.2%)
14 (0.2%)
This table shows that, out of 8628 man/days at sea, the crews had suffered
seasickness to one degree or another, and had been rendered less efficient as a
consequence, for 1179 man/days (13.7%). During these days at sea, 26 had been
calm, 26 had been moderately rough and 41 had been rough. In terms of man/days,
the incidence of seasickness in calm seas was 0.2%. In moderately rough sea
conditions the incidence had risen to 3.6% and in rough conditions, had reached
26.5%.
During the winter of 1979/80, Pethybridge (1982) carried out a survey among
the crews of 14 operational Royal Navy ships of different classes in order to
estimate both the incidence of motion sickness and any relationship of those data to
the size of the appropriate ships. He obtained 1746 completed questionnaires out of
a total of 2000 personnel, which in itself is a commendable and useful effort. The
incidence of seasickness increased as the sea conditions became worse, irrespective
of the type of ship on which the respondent had been serving at the time of the
survey. Few of the sailors had become seasick in calm seas. Some 25% of
crewmembers experienced seasickness in moderate seas and 69–70% in rough seas.
The average incidence of seasickness related to types of ships was reported as 50%
for guided missile destroyers, 55% for general-purpose frigates and survey ships,
65–70% for offshore patrol vessels and also for minehunters/minesweepers. In the
US Navy, the Naval Medical Information Center (1996) has reported that during the
calendar years 1980 through 1992, 489,266 new cases of motion sickness had been
diagnosed and a further 106,932 revisits had been recorded. This represents a
significant loss of effective manpower and funds.
Those who go on cruises and cross-channel ferries usually do so infrequently,
which reduces their chances of becoming habituated to the ship’s motion. Much
depends upon the sea conditions during the first 3 or 4 days of a cruise. For
example, Hill (1936) has estimated that over 90% of inexperienced passengers
became seasick in very rough conditions and some 25–30% became sick during the
first two or three days in moderate seas. Chinn (1951) has also reported that during
the first two or three days of an Atlantic crossing, in moderate seas, 25–30% of
passengers on liners became seasick.
Lawther and Griffin (1988) conducted a questionnaire survey of motion sickness
occurring on board passenger ferries. They designed a questionnaire that was both
clear and easily understood, as well as being quick to complete. Detailed questions
concerning motion sickness susceptibility were avoided. Data had been collected
from 20,029 passengers on a total of 114 voyages on nine vessels, which included
six ships, two hovercraft and one jetfoil, during rough weather conditions. In the
2.1 Seasickness
37
initial examination of their data, they pooled the results over all voyages and vessels
and found that 7% of the passengers had vomited at some time during the journey,
21.3% had felt “slightly unwell,” 4.3% had felt “quite ill” and 4.1% had felt
“absolutely dreadful.” Since they had deliberately sought rough weather, the percentage of seasickness was likely to have been higher than an overall figure for the
whole year, which would include periods when the seas would have been calm.
Nevertheless, Lawther and Griffin concluded that a figure of 1 in 14 for vomiting
and a feeling of illness in 1 in 3 passengers showed that seasickness was a significant problem in this situation. In another study, Lawther and Griffin (1986)
reported an incidence of emesis of approximately 40% among some 5000 passengers on cross-channel ferries. This study is mentioned again later in Chap. 4.
Turner and Griffin (1995) pointed out that only a few studies of the incidence of
seasickness have been based on long duration exposures at sea. They referred to the
3-day study by Wiker et al. (1979a, b) during which they found significant
covariance between the severity of motion sickness from questionnaire data and the
vessel’s encounter direction with regard to the primary swells. In summary, they
found that the incidence was higher on vessels with greater amounts of vertical
motion and the symptoms of seasickness were generally maximal when the ships
were experiencing some effects of head seas. Applebee et al. (1980) carried out a
similar study over 4 days on a 43 m Coast Guard Cutter and found that seasickness
was greatest when sailing into head seas and was least in either quartering seas or
following seas. Later, Applebee and Baitis (1984) reported that the incidence of
seasickness also varied with the relationship of the ship’s heading and the sea on an
82 m Coast Guard Cutter. Finally, Turner and Griffin drew attention to the seasickness data reported by Goto and Kanda (1977) from a 4 month voyage involving
35 sea cadets on a 97 m ship in the Pacific Ocean. They found that the symptoms of
seasickness had fallen logarithmically over days to 10% of the initial value over the
first 10 days at sea.
In their study, Turner and Griffin (1995) have taken advantage of the 1992–1993
British Steel Challenge 9 months, 28,000 miles yacht race to investigate the
importance of sea state, yacht heading relative to the sea, and duration of continuous exposure, in causing motion sickness. The race was divided into four parts,
each going on a westerly heading against the prevailing winds and ocean currents.
In order to ensure that the crews were able to race on even terms the fleet of 10 steel
Bermudian Cutters, 67 feet in length, had all been built to the same specifications.
Each yacht was sailed by 14 crewmembers including a professional skipper randomly chosen. Before joining the British Steel Challenge competition, the other
applicants had different levels of experience ranging from 9% (self-assessed as very
experienced) through 65% (little or no previous experience). The remainder considered themselves “quite experienced.” All of the potential crewmembers had been
given prior sea training ranging from 3000 to 5000 nautical miles, over a period of
2 years, in a prototype cutter.
Motion sickness questionnaires had been completed one week prior to the start
of the race, together with details on the occurrence of motion sickness during
training, sailing experience prior to joining the programme and relevant personal
38
2 Incidence of Motion Sickness
socio-demographic information. During the race itself, each member of the crew
was required to maintain motion sickness logbooks containing 24-hourly information on the occurrence of motion sickness and any use of anti-motion sickness
medication. Subsequently, all crewmembers had been requested to complete a
post-race questionnaire one week after the finish. This document provided further
details on the occurrence of motion sickness at any time during the training or the
race itself. The researchers calculated both an “illness incidence” (based on the
number of days ill divided by the number of days sailing 100) and a “vomiting
incidence” calculated in similar manner. The response rates across the various
yachts, particularly during the race, varied greatly from 0 out of 17 crewmembers to
13 out of 17 crewmembers. The post-race response had been much better. However,
Turner and Griffin suggested that the occurrence of motion sickness had not
influenced the rates of response for the questionnaires. They based their opinion on
the lack of significant differences in post-race reports between those who completed
or did not complete the motion sickness logs during the race or the pre-race
questionnaire.
Turner and Griffin compared the percentage of crewmembers who had reported
seasickness or vomiting during the pre-race training period and during each of the
four legs of the race. These data had been extracted from the pre-and post-race
questionnaires, presumably because of the low completion rates for the questionnaires during the race. They found a consistent decrease in the percentages for both
illness and vomiting from the pre-race responses to those across the four legs of the
race. The figures for “illness” diminished from 78% pre-race, with significant
decreases through 67% (1st leg), 55% (2nd leg), 47% (3rd leg), to 43% (final leg).
In the case of vomiting the significant figures were 62, 56, 34, 23 and 16%. There
was also a significant decline in the number of days on which illness and vomiting
had been reported. During the first leg, the average crewmember reported seasickness on 6.3% of days and vomiting on 2.9% of days. By the fourth leg, these
figures had dropped to 2.3 and 0.7% respectively. In addition, the crewmembers
had been requested to rate the frequency of occurrence of 14 different signs or
symptoms of motion sickness in their post-race reports, using a 4 point scale, as
follows: (0) = never experienced; (1) = occasionally experienced; (2) = often
occurred and (3) = usually occurred. Following a factor analysis of the symptom
frequency data, the researchers extracted four factors. These results were shown in
Table 1.1, Chap. 1.
Turner and Griffin noted that there was a wide inter-subject variability in terms
of habituation to sea motion, however, most had been free of motion sickness
responses by the 11th day of each leg. They also noted that sickness had been more
prevalent among crewmembers who used anti-motion sickness medications compared with those who had not. Conversely, as they pointed out this was likely to be
accounted for by the increase in the use of these medications among those
crewmembers that expected to be seasick. Further information on the drug
responses and the effect of drug motion, age and the sex of the individual are
discussed later in the appropriate part of this book. Turner and Griffen concluded
2.1 Seasickness
39
that during extended voyages, the occurrence of seasickness depended heavily on
the length of time spent at sea.
In a study involving more than 15,000 men, Tyler (1946) reported that the
overall incidence of seasickness on landing craft used for amphibious training had
been 35% among untreated personnel, of whom 13% were severely seasick. He also
reported that the incidence of seasickness had been high even in relatively calm
seas. During some trial runs in landing craft, in heavy seas, the incidence of motion
sickness reached 53%. There is still a high incidence of seasickness in current
shallow draft patrol craft in rough seas and also in troop-carrying air-cushioned
landing craft (LCACs). Seasickness remains a significant problem to this day as
newer ships are being designed with fewer crewmembers and therefore fewer
people available to replace those who are seasick. Chan et al. (2006) compared the
incidence of motion sickness between army troops and naval seamen at sea on small
boats in the monsoon period and found that the difference was of the order of
59.2%/38.3% (Army personnel vs. Sailors).
In the case of life rafts, which have particularly provocative motion profiles,
Money (1970) reported an incidence of seasickness as high as 99% in rough seas.
Even in moderate seas, symptoms of motion sickness occur relatively quickly.
Brand et al. (1968) reported on a particular life raft trial in which 55% of all subjects
had vomited. Only 24% remained free of symptoms after exposure to the effects of
artificial wave motion for a period of one hour. As previously included in Chap. 1,
Llano (1955) has noted that some 60% of water survivors complained of seasickness, which led him to believe that it has contributed to loss of life in many more of
those people than had been realised.
2.2
Airsickness
The incidence of airsickness also ranges widely according to circumstances, such as
aircraft types and the function of the mission that is involved, from a fraction of 1%
in large civil passenger aircraft to 100% during hurricane penetration flights in
individuals who have had no previous experience of such severe turbulence before
(Lederer and Kidera 1954).
The majority of people who suffer from airsickness when they first start learning
to fly adapt to the new environment within the first 15 h or so and their symptoms
disappear. This time scale varies with the particular phase of the flight-training
programme and the type of aircraft, since it depends largely on such variables as the
timing of the early acrobatic and spinning manoeuvres. Some student aviators have
a more prolonged history of airsickness than others and need further help and
encouragement. A smaller but very important group of trainees fails to respond to
early treatment despite the efforts of the flight instructors and medical officer and
become intractably airsick. The decrement of performance in these students can be
so severe that it critically affects their training progress, and their supervisors must
decide whether or not it is justifiable to allow them to continue flight training.
40
2 Incidence of Motion Sickness
Intractable airsickness represents a large economic loss. Not only are these
highly motivated and potentially valuable people on the verge of becoming training
failures, but they also have already cost a large amount of money in training hours
and supervisors’ time. For example, as long ago as 1985, Jones et al. estimated the
loss of a student pilot at 15 h to be over $15,000 and the loss of a trained flier at
around the half-million dollar mark. In 1994, a figure of three million pounds
sterling (approximately $4.5 US million) has been suggested as the value of an
experienced front-line RAF pilot. A successful anti-motion sickness training programme has great merit in terms of cost-effectiveness.
Rubin (1942) has quoted an incidence of 11% (ranging from 6 to 22% with
different training courses) for airsickness in a study of 837 cadets undergoing
primary flight training. Hemingway and Green (1945) studied the training records
of 2689 flight cadets and reported that 11% of the trainees had been sick one or
more times during their first ten flights. On the first flight, the incidence had been
5.3%, dropping to near zero by the tenth flight. Subsequently Hemingway (1946)
found that in the case of 178 flight cadets who suffered from airsickness and who
had completed ten one-hour flights, there had been a similar decrease in the incidence of airsickness by the tenth flight. A survey of flight instructors’ post-flight
reports showed that 38.7% of 577 RAF flight trainees had suffered from airsickness
at some time during their basic flight training on single-engine jet aircraft, usually in
the early stages (Dobie 1974). In 2008, Lucertini et al. reported on a study with
336 male and 40 female flight trainees in which the overall incidence of motion
sickness at basic flight training was 34.8%, with no differences between the sexes,
compared with the figure of 38.7% reported on by Dobie in 1974 for RAF male
students at Basic. In the Italian Air Force study the female trainees were slower
adaptors than the males (12.5% compared with 3.3% for the males). In more than a
third of the RAF cases, the degree of airsickness had been sufficiently severe and
protracted to be detrimental to the effectiveness off flight training or had cause
sorties to be abandoned altogether Table 2.2).
McDonough (1943) studied the incidence of airsickness among 380 navigation
cadets and found that 65% of them had reported being sick on one or more
occasions during a total of 4534 training flights. In a study at a combat bomber
crew-training unit, Green (Hemingway and Green 1945) recorded the incidence of
airsickness of 1006 experienced flight personnel. He found that 52% of
176 navigator-bombardiers had suffered from airsickness on one or more occasions
and 23% had been sick five or more times. He also recorded the incidence of
airsickness for other categories of flight crews as shown in Table 2.3. Overall,
Table 2.2 Incidence of
airsickness during basic flight
training (RAF), based on
instructors’ post-flight reports
on 577 trainees
No record of
airsickness
Mild
airsickness
Severe
airsickness
61.3%
24.1%
14.6%
Mild airsickness = does not materially affect the student’s ability
to absorb instruction in flight
Severe airsickness = results in a wastage of training time and
causes a number of sorties to be abandoned prematurely
2.2 Airsickness
Table 2.3 Incidence of
airsickness for the different
categories of flight
crewmembers at a combat
bomber crew training unit
41
Flight crewmembers category
Incidence of airsickness (%)
Radio-gunners
Navigator-bombardiers
Engineer-gunners
Pilots
Armorer-gunners
32
19
16
13
11
he found that the average incidence of airsickness for all categories of flight
crewmembers at that training unit had been 17%.
In reviewing these data, Tyler and Bard (1949) suggested that this increased
incidence of airsickness among these particular crewmembers might have been
partly due to the fact that a number of them had already been eliminated from pilot
training due to chronic airsickness. However, Tyler and Bard also pointed out that
their particular duties involved “conditions of vision and posture that tend to
facilitate the development of motion sickness.” Similar differences in the incidence
of motion sickness are still seen in large multi-seat aircraft, as we shall later when
discussing B1-B crewmembers. In addition to bodily posture per se the
crewmembers’ location on the aircraft is also important. This and other features are
not only significant in aircraft, but in all forms of vehicular motion, as I shall
discuss later in the appropriate section of Chap. 9.
Hixson et al. (1980) collected flight data from a total of 1833 sorties flown by
134 VT86-AJN students who had undergone training for various weapon operation
and navigation duties in attack and anti-submarine warfare aircraft. They found that
some 55% of the students reported that they had been airsick on one or more flights;
28% had vomited on one or more flights, and 30% acknowledged that their flight
performance had been degraded by airsickness on one or more flights. In terms of
the total number of sorties flown, airsickness had been reported in 8.6% of the
sorties, vomiting in 3.7%, and degradation in task performance in 3.4%.
A study of US Navy officers undergoing flight training for various non-pilot
crew duties has shown the mean incidence of airsickness to be 13.5% of all flights.
This caused a decrement in trainee performance in 7.3% of flights (McDonough
1943). In a later paper, Hixson et al. (1983) reported the incidence and severity of
airsickness that had occurred in 14 different fleet readiness squadrons. These data
were based on the experiences of 372 naval flight officer students who had flown a
total of 8325 sorties during this part of their flight training. Treating this entire
population as a single group, they found that airsickness was reported during
637 (7.65%) of the total number of flights, vomiting had occurred on 252 sorties
(3.30%), and there had been a degradation of performance due to airsickness on 303
flights (3.64%). These data showed significant differences according to the type of
training being carried out for specific aircraft types. It was particularly noticeable
that the incidence of airsickness during flight readiness squadron training in the P-3
aircraft had been especially high. The report discussed these variations based upon
differences in the flight syllabi associated with each phase of training. I found a
similar situation while evaluating the incidence of airsickness during flight training
42
2 Incidence of Motion Sickness
in the RAF (Dobie 1974). Regarding civilian flight training, Lindseth and Lindseth
(1992) reported that in their study, 28.1% of civilian student pilots had experienced
symptoms of airsickness.
Littauer (1943) has investigated the incidence of motion sickness among airborne troops. He found that 80% of those in transit on a five-hour flight in planes
and gliders had become sick. Park (1943) reported an average incidence of 35%
during what he called “glider manoeuvres”. Johnson and his colleagues (Johnson
et al. 1951; Johnson and Mayne 1953) subsequently addressed the issue of
restricting head movements as a means of reducing the incidence of airsickness
among airborne troops in transit.
During the period 1962–1969, Ryback et al. (1970) investigated 49 flight
crewmembers who had been referred to them; 44 with a diagnosis of motion
sickness and 5 others for different reasons, but found to be suffering from this
malady. Typically they came from Strategic Air Command, had less than 1000
flight hours and were aged between 20 and 29 years. Thirty-six of the cases were
navigators, 11 were pilots and 2 had non-rated duties. Seventy-one percent of these
individuals had given a previous history of motion sickness on carnival rides and
occasionally in the air before joining the United States Air Force. Ryback et al.
concluded that motion sickness could result from what they called primarily
“organic” or psychiatric” causes or a combination of both. In their opinion, far from
being malingerers, the majority of their patients suffering from motion sickness had
an “organic” basis for the malady. They listed 8 “organic” factors: symptoms in
turbulence or during aerial acrobatic maneuvers; migraine-like headaches; a history
of syncope; a history of middle ear infection; a history of head trauma; washed out
of pilot training because of airsickness; decrease in ability to see the horizon
(navigators); and tendency to become ill. It seemed that a number of these individuals had a history of events that might well have caused clinical disabilities. It is
interesting to note that the majority of them were navigators, many of whom had
failed pilot training, so that motivational factors perhaps played a significant role in
their problems. I have noticed such a pattern when dealing with graduate aircrew, as
distinct from flight trainees. Motion sickness may be used as a screen to cover
disappointment at not qualifying for a chosen career role.
Strongin and Charlton (1991) carried out an assessment of airsickness in an
operational setting in which 88 B1B B-52H male crewmembers had completed the
“B1B Airsickness Research File” questionnaire. This was an eight-item survey in
three parts. The first part consisted of an introductory explanation of the symptoms
of airsickness and a statement that represented anonymity for the volunteer
crewmembers. The second part requested demographic information, namely, crew
position and experience level, as well as the number of both total sorties and
low-level flights that had been flown in the last thirty days, and the number of
flights on which the subject was airsick. The last part of the questionnaire required
information about the duration of any airsickness and the effect it had on the
performance of the reporting crewman and any others he might have observed.
The authors reported that the percentage of flights in which airsickness was
experienced has been directly related to crew position, rather than either aircraft
2.2 Airsickness
43
type, or the interaction of crew position and aircraft type. They noted, however, that
the severity of in-flight incapacitation was significantly predicted by the combination of crew position, aircraft type, and the amount of flight time on bomber
aircraft. Overall, this study revealed that pilots, B1-B crewmembers and
crewmembers with less bomber experience, were the least affected adversely by
motion sickness. Non-pilots in both types of aircraft reported that airsickness had
been a frequent occurrence. Finally, Strongin and Charlton have opined that
experienced crewmembers were more likely to report that their airsickness resulted
in a decrement in the performance of their duties.
Turner et al. (2000) investigated the incidence of airsickness among passengers
in short-haul turboprop aircraft. A motion sickness questionnaire survey of
923 passengers had been implemented on a total of 38 flights. The modified survey
questionnaire was developed for a previous road transport study (Turner and Griffin
1999). The approximate durations of the flights over the various routes were
between 35 and 70 min.
The results of this study showed that in general, 14.2% of respondents felt
“slightly unwell”, 1.6% “quite ill” and 0.4% “absolutely dreadful.” In terms of
separate journeys, the incidence of airsickness based on the percentage of passengers giving an illness rating greater than zero ranged from 0% to approximately
48% and tended to occur in the early part of the flight. Turner et al. concluded that
the overall incidence of airsickness was comparable with that which had been
predicted by previous workers (Benson 1978). Less that 1% of the passengers
reported vomiting and some 16% have recorded symptoms of airsickness. As they
pointed out, that was a lower percentage than they had published for seasickness
and on land transport (Turner and Griffin 1999; Lawther and Griffin 1986).
2.3
Space Adaptation Syndrome
Cowings et al. (1988) have described the space adaptation syndrome as a motion
sickness-like disorder that affects up to 50 of all people who have been exposed to
the microgravity of space. The incidence and severity of space sickness also varies.
It has become troublesome with the advent of larger space vehicles that allow the
crews greater freedom of movement, particular head movement, causing increased
vestibular stimulation. Homick wrote in 1984 that space motion sickness, was now
called the space adaptation syndrome (SAS) was a special form of motion sickness
experienced by some astronauts during the early days of exposure to the space
environment and is an operationally relevant biomedical problem to the space flight.
Homick (1979) commented that the space adaptation syndrome (space motion
sickness) had been commonly experienced by many crewmembers during the early
phase of space flight missions.
In view of the serious implications associated with space sickness, Homick et al.
(1984) reiterated the opinion that it constituted a significant problem for manned
space flight. In order to better predict, prevent and treat space motion sickness,
44
2 Incidence of Motion Sickness
the NASA-Johnson Space Center initiated a systematic, long-range programme to
collect operational data on all crewmembers flying Space Shuttle missions. Before
each flight, investigators obtained information from a motion experience questionnaire, performed laboratory tests of individual susceptibility to motion sickness
induced by cross-coupled (Coriolis) stimulation, and evaluated the efficacy of
anti-motion sickness drugs, together with any significant side effects. During space
flights, each member of the crew maintained a daily record of motion sickness,
other vestibular-related sensations and any use of anti-motion sickness medications.
Other relevant data were also been obtained post-flight.
Homick and his co-workers had reported in 1984, an incidence of 48% for space
motion sickness during the first nine Shuttle missions. The severity of symptoms
and signs ranged widely, with general malaise, anorexia, nausea and vomiting being
the most common. Self-induced head movements and unusual visual orientation
attitudes seemed to constitute the main provocative stimuli. Although many
crewmembers had used anti-motion sickness medication, it was found to give only
limited protection. Complete recovery from the various symptoms of motion
sickness occurred by the third or fourth day of the mission. Homick et al. also
reported the absence of a statistically significant correlation between the
ground-based Coriolis test and space motion sickness. Despite the occurrence of
this malady during the early part of the mission they reported that this did not have
any significant adverse effect on the objectives of Shuttle missions. Apparently, the
only exception had been a one-day postponement of a scheduled space walk on the
fifth mission.
Davis et al. (1988a) reported that motion sickness in microgravity is a persistent
and frequent operational problem. Oman et al. (1984) recorded that 50% of crew
personnel have experienced space sickness. Jennings et al. (1988) pointed out that
space motion sickness is an important problem, particularly for short duration space
flight, and reported an incidence of about 71%. Clearly, the duration of the flight is
an important variable in this situation, because the majority of astronauts who
experience motion sickness in space do so during the first 72 h of the mission. As a
consequence of this, any extra-vehicular activity is planned to take place after the
third flight day so that any members of the crew required for this activity who have
been suffering from motion sickness would have had the opportunity to recover.
Davis et al. (1988b) summed up the incidence of motion sickness in various
space vehicles, as: Apollo, 35%; Skylab, 60%; Space Shuttle, four orbital test
flights, 50% (four out of eight crew members). In the Soviet manned space flight
programmes, the figures that had been given were as follows: Salyut-6/Soyuz, 44%;
Salyut 7, 40%; earlier Voskhod and Soyuz flights, 50–60%. Clearly this is a serious
problem, which has been described by Davis et al. as “a persistent operational
medical problem,” which “has been called the most clinically significant medical
phenomenon during the first several days of space flight.”
These workers have then determined the incidence and severity of space motion
sickness during 24 flights of the Space Shuttle programme. They gave a motion
sickness questionnaire to all crewmembers during a verbal post-flight debriefing
with the flight surgeon. This has usually taken place within the first hour after
2.3 Space Adaptation Syndrome
45
landing. The questionnaire had been developed at the NASA-Johnson Space Center
(JSC) in 1984. The severity of crewmembers’ motion sickness responses was
graded according to criteria developed at the JSC (Table 2.4), as being mild,
moderate or severe.
The incidence of space motion sickness for 85 crewmembers during a seven-day
first Shuttle flight was 67% (57 cases). Of these, 26 were classified as being mild
cases (30%), 20 as moderate (24%) and 11 had been considered to be severe (13%).
Differences were observed between males and females, crew positions (commander, pilot, mission specialist, etc.) and age groups, however these have not been
statistically significant. Davis et al. (1988b) stated that these differences indicated
that future research into the mechanisms, prevention and treatment of motion
sickness during space flight was required. Regarding those 26 crewmembers who
had made a second flight on the Shuttle, the incidence of their space motion
sickness had dropped down to 46%, compared to 62% on their first flight. In fact,
analysis of the data for 26 pairs of crewmembers showed that the reduction in
incidence from the first to the second flight was not significant. however. Nine of
the crewmembers (35%) showed a reduction in the severity of their motion sickness
between the first and second flights, although there had been no significant difference in the mean time between flights for those crewmembers who experienced
space motion sickness when compared with those who did not. Davis et al. concluded that differences in training and flight experience of crewmembers might
explain these observations; it is felt, however, that the experience was perhaps more
significant than the training.
More recently, Beck and Nicogossian (1992) have stated that space motion
sickness affects approximately 74% of first-time shuttle flyers in the NASA space
programme. This is a higher figure than the 67% reported by Davis et al. (1988b) four
years earlier, but again, the authors gave no particular explanation for this apparent
7% increase in the previous figure from the incidence recorded only a few years
before; their opinion on this increase might well have been extremely useful.
Table 2.4 Space motion sickness categorisation
Grade
Symptoms
None (0)
No signs or symptoms reported, with exception of mild, transient headache or
mild decrease in appetite
One to several symptoms of a mild nature; may be transient and only brought on
as the result of head movements; no operational impact; may include single
episode of retching or vomiting; all symptoms resolved in 36–48 h
Several symptoms of a relatively persistent nature; may wax and wane; loss of
appetite; general malaise, lethargy, and epigastric discomfort may be most
dominant symptoms; includes no more than two episodes of vomiting; minimal
operational impact; all symptoms resolved in 72 h
Several symptoms of a relatively persistent nature which may wax and wane; in
addition to loss of appetite and stomach discomfort, malaise and/or lethargy are
pronounced; strong desire not to move head; includes more than two episodes of
vomiting; significant performance decrement may be apparent; symptoms may
persist beyond 72 h
Mild (1)
Moderate (2)
Severe (3)
46
2.4
2 Incidence of Motion Sickness
Simulator Sickness
In their 20 month questionnaire study, involving 3690 “hops”, Kennedy et al.
(1991) recorded data from subjects on two TH-57, primary helicopter flight trainers,
Devices 4 and 2, immediately after exiting the simulator. They reported that
roughly half of the subjects showed virtually no simulator sickness, whereas the
remainder reported symptoms varying from mild to severe. They carried out
analyses using arithmetic means and, because of the marked skewness of the
results, used 75th percentile scores. They had done so on the basis that it was in
effect the midpoint in terms of those subjects who suffered from simulator sickness.
They classified the simulator sickness symptoms according to three major factors
derived from their large database, which they had considered to have a theoretical
relevance because of their origins, namely, neurovegetative, vestibular and oculomotor responses. They also recorded a total score that represented the subject’s
general feeling of discomfort. By this method, they found that adaptation to the
simulation occurred over a series of hops and that after four hops, the incidence and
severity of simulator sickness has been very slight. They also found that the two
simulators they reviewed in this study had virtually identical patterns in terms of the
symptoms they produced. The main problems had been nausea and vomiting. They
took this to mean that these responses were related to the motion environment rather
than what they called “visuomotor or disorientation issues.” For those reasons, they
concluded that in order to reduce the incidence of motion sickness in these particular devices, attention should be paid to the motion base rather than the
visual-inertial reactions.
The incidence of simulator sickness varies with the type of simulator and can be
widespread. Kennedy et al. (1989) recounted a study involving 10 US Navy and
Marine Corps flight simulators in which some 20–40% of pilots reported at least
one symptom of simulator sickness. Later, Kennedy et al. (1990) further reported a
study involving 2500 simulated flights where the incidence varied from 10 to 60%
across the 10 simulators they surveyed.
Money (1991) has also noted that the incidence of simulator sickness varied
considerably with the particular simulator, the exercise that was being carried out,
and the various criteria being used to diagnose simulator sickness. He referred to the
report by Kennedy et al. (1990), mentioned in the previous paragraph, in which
they recorded that the incidence of simulator sickness varied from 10 to 60%. He
observed that this order of incidence has been reported in many other publications.
Money summarised this question of incidence by stating that 10% of pilots had
experienced nausea in simulators whereas some 25% had reported eyestrain.
Kennedy et al. (1984) pointed out that simulator sickness is a relatively new
problem that was first reported in relation to aircraft simulators and then in driving
simulators. They observed that although some training simulators have been in
existence for some time, wide field of view visual systems had only been used in
simulators in recent times. They believed that the introduction of the wide field of
view corresponded closely with the onset of simulator sickness but have not gone
2.4 Simulator Sickness
47
so far as to say that it was the cause of this malady. They reviewed numerous
studies and emphasized the main features that emerged, as follows:
There is little difference in the incidence between fighter, transport and helicopter simulators; simulator sickness is reported in both fixed and moving-base
simulators;
• The occurrence of simulator sickness is reported with various types of visual
systems including flat-screen, dome and computer image generation; simulator
sickness is closely associated with wide field of view simulation;
• The greater the intensity and longer the duration of exposure, the greater is the
incidence of sickness;
• The illumination of the screens is dim or at intermediate light levels;
• Visual and inertial lags are reported;
• The incidence of simulator sickness is greater in experienced pilots than in
students;
• The reported incidences range from 11 to 88%;
• Reference to adaptation is made in 30% of the reports;
• The most common symptoms are nausea, dizziness, and muscular
incoordination;
• There is evidence that the symptomatology reports are incomplete.
These workers carried out a field experiment involving 36 qualified Naval
aviators who had flown SH-3 helicopter simulators and another 28 qualified Naval
aviators who have flown SH-2 helicopter simulators. Performance tests were carried
out to investigate possible decrements in psychomotor performance due to exposure
to the simulators, using an Air Combat Maneuvering video game. Two postural
equilibrium measures had also been included before and after each simulator session. These were the Walk-Heel-to-Toe-Eyes-Closed (WHTEC) and the Standon-Preferred-Leg Eyes-Closed (SOPLEC) tests.
They found that there was no difference in the results obtained between the two
different types of simulators and consequently they pooled the data. The scores
obtained for both pre- and post-ataxia tests had not been significantly different nor
indeed had the performances been degraded on the video games. As far as symptoms were concerned, 13% of the pilots reported a considerable amount of discomfort. Nearly 40% of subjects reported two or more symptoms of motion
sickness and 80% indicated that they experienced one or more symptoms. The
scores obtained from motion sickness questionnaires were only mildly predictive of
those who experienced greater difficulty. These workers concluded that simulator
sickness was a problem, as yet of unknown magnitude. Further studies needed to
pay greater attention to the nature of the stimulus, including such things as definitions of the scenario, measures of both visual and inertial lags and the resonant
heave frequency of the particular simulator.
Hettinger et al. (1990) carried out a study in which stationary subjects passively
reviewed three different computer-generated flight scenarios that had been shown to
induce simulator sickness in subjects who were susceptible. Each of these scenarios
48
2 Incidence of Motion Sickness
lasted for 15 min and there were 18 male subjects ranging in age from 18 to
35 years. Prior to exposure, subjects had completed a motion sickness questionnaire
(MSQ) (Wiker et al. 1979a,b). The MSQ was repeated once during each of two
5-min rest intervals and finally on completion of the last motion display. The
projection system in the simulator provided a field of view of 40° vertical by 80°
horizontal, on a large interior projection screen that was 10.5 ft. high, 21 ft. long,
with a 15-foot radius of curvature. The display showed aerial self-motion through
mountainous country. A suitable baffle had occluded most of the stationary visual
information sources.
The data from only 15 subjects had been analyzed, since there were technical
and instructional problems in the other three. Ten of the subjects were classified as
having suffered from motion sickness based on a score of four or more on their final
motion sickness questionnaires. In view of the cumulative nature of motion sickness, these workers had only reported the results that followed the second and third
displays.
The subjects were asked to indicate if they had experienced any feelings of
illusory self-motion (vection). In order to ensure that the subjects had understood
this concept, they were given detailed written instructions on the definition of the
illusion of vection. Vection was described as a feeling as if moving in an automobile or an aeroplane. The subjects had been asked to rate the strength of this
illusion indicating no self-motion, weak feelings, moderate feelings and very strong
feelings of self-motion. These magnitude estimates were made by means of
adjustments on a hand-held potentiometer to one of four number locations from
zero to three. Concerning reports of vection, they found that most subjects had
either reported a lot of vection or none at all. Regarding simulator sickness in period
three, these workers categorised the subjects who had reported motion sickness at
level four or higher as being motion sick. Those with scores of three or less were
not considered to be motion sick. They found that of the five subjects who had not
reported vection during periods two or three, only one of them had become sick.
Of the remaining ten subjects who had experienced vection, eight of those had
become motion sick. They concluded that this relationship between vection and
simulator sickness suggested that those visual displays that produced vection were
more likely to produce simulator sickness.
Reason and Diaz (1971) have carried out an interesting simulator study that
involved passive rather than active observers. Sixteen male and fifteen female
undergraduates and technical staff, aged 17–23 years, were used as subjects. In this
experiment, they used a car simulator (Sim-L-Car) that was controlled by the
investigator while the subject, who had been seated alongside him, passively
observed the visual display through the window screen. All of the subjects completed a motion sickness questionnaire at the end of the experiment. Subjects were
asked to estimate the average number of hours per week they spent as car passengers and as car drivers. Each subject was driven over a standard simulated
course for 10 min. Half of the subjects wore so-called “blinkers.” These consisted
of an oval rubber tube held by the subject over his or her eyes in order to exclude all
but the projection screen, which measured 12′ by 6′, from the subject’s visual scene.
2.4 Simulator Sickness
49
There were two main dependent measures in this study. First, a Well-Being
Scale that consisted of magnitude estimates on an 11-point scale, ranging from
0—“I feel fine” to 10—“I feel awful, just like I’m about to vomit.” The second
measure was a Symptom Score that had been derived from a standardised symptomatology checklist. To achieve the overall score, any signs or symptoms of
motion sickness were categorised as mild, moderate or severe and given the
appropriate weighting of 1, 2 or 3. The final symptom score was obtained by adding
the total of these individual weightings. In addition, the subjects were also asked to
evaluate the realism of the driving this particular simulation on an 11-point scale,
that varied from 0—“Not at all like a real car” to 10—“Just like a real car.”
Apparently there were no ill effects recorded by either the Well-Being Rating or
the Symptom Score in only 3 of the 31 subjects. The most frequently reported
symptom, that was recorded by both men and women, was dizziness. Whereas the
next most common symptoms were body warmth, headache, stomach awareness
and nausea. The only difference recorded between the male and female subjects was
the presence of pallor, which has been seen much more often in women than in
men. With the exception of increasing salivation, all of the symptoms occurred
more commonly in the female subjects. Sixteen of the subjects had worn blinkers
that restricted their visual field to the 12′ by 6′ moving visual scene that was placed
6′ from the occupants. This represented a visual angle of only 26°. Neither males
nor females reported any differences between those with restricted visual fields and
those without. That perhaps reflected the narrowness of the visual angle.
Susceptibility to simulator sickness in both men and women was found to be
positively related to the amount of previous experience with travel in an automobile
both as passenger and driver. They found that for both men and women the relationships between simulator sickness and driver experience has been better than for
those with passenger experience. In conclusion, Reason and Diaz found that 28 of
the 31 subjects reported a reduction in well-being. Women were more susceptible
than men. Previous experience in a car had correlated with the degree of simulator
sickness. The blinkers appeared to have no effect.
2.5
Sickness Related to Virtual Reality Systems
Kennedy et al. (1992) have pointed out that virtual reality systems gave rise to
malaise and discomfort that resembled motion sickness. They did stress, as discussed in the previous section dealing with simulator sickness, that the latter created
symptoms that were more related to ocular-motor symptoms than actual vomiting.
They suggested that their method of evaluating simulator sickness would have a
useful input into the study of discomfort produced by virtual environments. They
concluded that problems with simulator sickness would generalise to virtual reality
systems that included simulated self-motion. The subsets identified were those
relating to nausea, oculomotor disturbances and disorientation. In view of the
50
2 Incidence of Motion Sickness
similarity between conventional simulators and virtual reality, the workers’ results
and comments would seem to have been highly appropriate.
Regan and Price (1994) investigated the frequency and severity of side effects
associated with the use of an immersion virtual reality system. In that system, the
user wore a head-mounted display that projected the virtual world through one or
two small screens directly in front of the subject’s eyes and gave the user the
illusion of being immersed in the virtual world. Since 1993, there has been considerable concern about the potential side effects of immersion in virtual reality.
This has arisen because of anecdotal reports of the side effects of virtual reality, as
well as numerous reports regarding simulator sickness.
Regan and Price stated that 61% of the 150 subjects in their study reported
symptoms of malaise at some point during a 20-min immersion in virtual reality and
a 10-min post-immersion period. Although these data were obtained from one
particular virtual reality system, they argued that the results could be generalised to
other such displays.
Kolasinski (1995) have defined virtual reality as a “three dimensional, interactive, realistic, real-time computer generated simulation providing direct input to the
senses via a head-mounted display (HMD), Binocular Omni-Oriented Monitor
(BOOM), DataGlove and similar devices.” They pointed out that, at the time of
writing, not all of these features had been fully realised. They stressed that the close
and direct association between simulator sickness and sickness caused by exposure
to virtual reality and that both of these maladies were classes of visually-induced
motion sickness. Kolasinski et al. reported that their early research into the use of
virtual environments to provide training scenarios had caused some trainees to
experience simulator sickness. The symptoms were similar to motion sickness,
namely, general discomfort, drowsiness, fatigue, apathy, headache, increasing
salivation, sweating, disorientation, stomach awareness, nausea and vomiting.
Additionally, subjects have been seen to exhibit pallor. They also pointed out that
postural instability and flashbacks have been recorded. These workers have identified and discussed the three main factors that they considered to be involved in
causing simulator sickness when using virtual environments, namely, those relating
to the individual, the simulator and the simulated task. This is a useful review of the
problems concerned with the use of virtual reality systems, and identifies, in some
detail, areas for future research into this particular type of simulator sickness.
Witmer and Lampton (2000) carried out 15 experiments involving 690 subjects
in a study investigating the value of navigation aids for “improving configuration
knowledge acquisition in a VE [virtual environment].” They used a 16-item
Simulator Sickness Questionnaire (SSQ) (Kennedy et al. 1993) to identify and
quantify symptoms of simulator sickness. They found that the symptoms of VE
sickness was so severe that 8.4% of the candidates withdrew from the experiments;
the wastage rates varied from zero—25%. In those with the highest withdrawal
rates, the symptomatology scores were generally much higher for subjects who
withdrew before the end, as expected (Fig. 2.1).
2.6 Motion Sickness in Other Forms of Provocative Motion
51
Fig. 2.1 Simulator sickness questionnaire (SSQ) scores for subjects who completed or withdrew
from experiments
2.6
Motion Sickness in Other Forms of Provocative
Motion
In other forms of provocative motion, the situation is very similar. For example,
Reason (1967) has surveyed 300 British undergraduates of both sexes and has
found that 58% experienced nausea related to motion while traveling in automobiles and 33% reported that they had vomited (for whatever reason) in automobiles
before the age of 12 years. Between the ages of 12 and around 20 years, 47% of
these students had experienced nausea and 14% had vomited while riding in
automobiles. The problem with reporting the incidence of motion sickness accurately, whatever the mode of transport, is that in some cases the cause of sickness
may have been unrelated to the provocative motion. Chinn and Smith (1953) have
reviewed many thousands of motion sickness questionnaires and commented that a
very large proportion of the population find the word amusement in the phrase
amusement park rides to be “something of a misnomer.” Motion sickness is very
common and the incidence and severity are very variable. Reason (1967) has
observed that for the population as a whole, automobiles, buses and ships have been
most likely to cause motion sickness, whereas small boats and trains have been
found to be the least provocative. Kaplan (1964) has reported a study in which there
were 485 documented cases of motion sickness among 371,261 passengers on the
Baltimore and Ohio Railroad, giving an average incidence of 0.13%. There has
been, however, anecdotal evidence that with the introduction of high-speed trains
having tilting carriages and higher acceleration on bends, the incidence of motion
sickness could become much greater. Benson (1988) has suggested that it could be
at least an order of magnitude greater than occurs on conventional passenger trains.
Car sickness is a very common complaint and I have helped many people to
overcome this problem using cognitive-behavioural desensitisation training which
52
2 Incidence of Motion Sickness
I shall be discussing in some detail in Chaps. 12 and 13. Perrin et al. (2013)
discussed this motion sickness problem as it affected male and female co-drivers in
rally cars; however, none of the people whom I managed happened to be co-drivers
who experienced a variety of high speed accelerations in that sport. They found that
reading a book in a car or when in a rear seat created high incidence problems as is
the case with passengers in ordinary cars and stress, on-board smells and high
temperatures were particularly bad.
2.7
Summary
• Seasickness is the most common form of motion sickness and is also extremely
variable according to the individual and situation.
• The most provocative frequency is around 0.2 Hz, but this must also be
accompanied by at least a medium amount of acceleration.
• The severity of airsickness is also very variable, according to crew position,
aircraft type, the individual’s amount of flight time and his or her early experiences in flight.
• The majority of flight trainees usually adapt to airsickness in about 15 h of
training. Intractable airsickness, however, represents a huge economic loss,
especially in military environments.
• RAF flight instructor reports have shown that some 39% of flight trainees suffered from airsickness at some time during their basic flight training on
single-engine jet aircraft.
• Reports show that 28% of civilian student pilots have suffered from motion
sickness.
• Space adaptation syndrome is a motion sickness-like disorder associated with
microgravity in space and commonly experienced by about 60–70% of people
during the early phase of space flight missions.
• Astronauts usually adapt to space motion sickness over a period of approximately 72 h
• Simulator sickness, a relatively new problem, varies with the type of simulator,
the exercise that is being carried out, various criteria used to diagnose simulator
sickness and can be widespread; field of view may be significant.
References
Applebee TR, Baitis EA (1984) Sea keeping investigation of the U.S. Coast Guard 270 ft medium
endurance cutter Bear (WMEC 901). Report DTN SRDC/SPD-1120-01, David Taylor Naval
Ship Research Center, Bethesda
Applebee TR, McNamara TM, Baitis EA (1980) Investigation into the sea-keeping characteristics
of the U.S. Coast Guard 140 ft WTGB class cutters: sea trial aboard the USCGC Mobile Bay.
Report DTN SRDC/SPD0938-01, David Taylor Naval Ship Research Center, Ship
Performance Department, Bethesda
References
53
Barlow LN (ed) (1946) Charles Darwin and the voyage of the Beagle. Philosophical Library, New
York
Beck BG, Nicogossian AE (1992) Use of injectable Promethazine to decrease symptom scores of
space motion sickness. Aviat Space Environ Med 63:387
Benson AJ (1978) Motion sickness. In: Dhenin G, Ernsting J (eds) Aviation medicine:
physiological and human factors. Tri-Med Books Ltd., London
Benson AJ (1988) Motion sickness. In: Ernsting J, King P (eds) Aviation medicine, 2nd ed.
Butterworth-Heinemann Ltd., Oxford
Brand JJ, Colquhoun WP, Perry WLM (1968) Side-effect of L-hyoscine and cyclizine studied by
objective tests. Aerosp Med 39:999–1002
Chan G, Moochhala SM, Zhao B, Yeo W, Wong J (2006) Int Marit Health 1–4
Chinn HI (1951) Motion sickness in the military service. Mil Surg 108:20–29
Chinn HI, Smith PK (1953) Motion sickness. Pharmacol Rev 7:33
Cowings PS, Toscano WB, Kamiya J, Miller NE, Sharp JC (1988) Autogenic feedback training as
a preventive method for space adaptation syndrome on Space-Lab 3. Aviat Space Environ Med
59:481 (abstract)
Davis JR, Vanderploeg JM, Stewart DF, Santy PA, Logan JS (1988a) Summary of motion
sickness experience on 24 shuttle flights. Aviat Space Environ Med 59:467 (abstract)
Davis JR, Vanderploeg JM, Santy PA, Jennings RT, Stewart DF (1988b) Space motion sickness
during 24 flights of the space shuttle. Aviat Space Environ Med 59:1185–1189
Dobie TG (1974) Airsickness in aircrew. AGARDOGRAPH No. 177, North Atlantic Treaty
Organization Advisory Group for aerospace research and development, Neuilly-sur-Seine,
France
Dobie TG, May JG, Fisher WD, Bologna NB (1989) An evaluation of cognitive-behavioral
therapy for training resistance to visually-induced motion sickness. Aviat Space Environ Med
60:307–314
Goto D, Kanda H (1977) Motion sickness incidence in the actual environment. In: Proceedings of
the United Kingdom Informal Group meeting on human response to vibration, UOP Bostrom,
Northampton, 7–9 Sept 1977
Hemingway A (1946) Selection of men for aeronautical training based on susceptibility to motion
sickness. J Aviat Med 17:153
Hemingway A, Green EL (1945) Incidence of airsickness in cadets during their first ten flights.
Project 170, report no. 5, AAF School of Aviation Medicine, Randolph Field, Texas
Hettinger LJ, Berbaum KS, Kennedy RS, Dunlap WP, Nolan ND (1990) Vection and simulator
sickness. Milit Psychol 2(3):171–181
Hill J (1936) The care of the sea-sick. Br Med J II:802–807
Hixson WC, Guedry FE, Holtzman GL, Lentz JM, O’Connell PF (1980) Airsickness during naval
flight officer training: advanced squadron VT86-AJN. NAMRL-1267, Naval Aerospace
Medical Research Laboratory, Pensacola
Hixson WC, Guedry FE, Lentz JM, Holtzman GL (1983) Airsickness during naval flight officer
training: fleet readiness squadrons. NAMRL1305, Naval Aerospace Medical Research
Laboratory, Pensacola
Homick JL (1979) Space motion sickness. Acta Astronau 1259–1272
Homick JL, Reschke MF, Vanderploeg JM (1984) Space adaptation syndrome: incidence and
operational implications for the space transportation system program. In: Motion sickness:
mechanisms, prediction, prevention and treatment. AGARD conference proceedings no. 372,
North Atlantic Treaty Organization Advisory Group for aerospace research and development,
Neuilly-sur-Seine, France, vol 36, pp 1–6
Jennings RT, Davis JR, Santy PA (1988) Comparison of aerobic fitness and space motion sickness
during the shuttle program. Aviat Space Environ Med 59:448–451
Johnson WH, Mayne JW (1953) Stimulus required to produce motion sickness: restriction of head
movement as a preventative of airsickness—field studies on airborne troops. J Aviat Med
24(400–411):452
54
2 Incidence of Motion Sickness
Johnson WH, Stubbs RA, Kelk GF, Franks WR (1951) Stimulus required to produce motion
sickness. 1. Preliminary report dealing with importance of head movements. J Aviat Med
22:365–374
Kaplan I (1964) Motion sickness on railroads. Ind Med Surg 33(1):648–651
Kennedy RS, Frank LH, McCauley ME, Bittner AC, Root RW, Binks TA (1984) Simulator
sickness: reaction to a transformed perceptual world VI. Preliminary site surveys. In: Motion
sickness: mechanisms, prediction, prevention and treatment, AGARD-CP-372, NATO/
AGARD, Neuilly-sur-Seine, pp 34, 1–11
Kennedy RS, Lilienthal MG, Baltzley DR, McCauley ME (1989) Simulator sickness in US Navy
flight simulators. Aviat Space Environ Med 60(1):10–16
Kennedy RS, Hettinger LJ, Lilienthal MG (1990) Simulator sickness. In: Crampton GH
(ed) Motion and space sickness. CRC Press, Inc., Boca Raton, pp 317–341
Kennedy RS, Smith MS, Jones SA (1991) Variables affecting simulator sickness: report of a
semi-automatic scoring system. In: Proceedings of the sixth international symposium on
aviation psychology, Columbus
Kennedy RS, Lane NE, Lilienthal MG, Berbaum KS, Hettinger LJ (1992) Profile analysis of
simulator sickness symptoms: application to virtual environment symptoms. Presence:
Teleoperators Virtual Environ 1(3):295–301 (The Massachusetts Institute of Technology)
Kennedy RS, Lane NE, Berbaum KS, Lilienthal MG (1993) A simulator sickness questionnaire
(SSQ): a new method for quantifying simulator sickness. Int J Aviat Psychol 3(3):203–220
Kolasinski EM (1995) Simulator sickness in virtual environments. Technical report 1027, U.S.
Army Institute for the Behavioral and Social Sciences, May 1995
Lawther A, Griffin MJ (1986) The motion of a ship at sea and the consequent motion sickness
amongst passengers. Ergonomics 29(4):535–552
Lawther A, Griffin MJ (1988) A survey of the occurrence of motion sickness amongst passengers
at sea. Aviat Space Environ Med 59:399–406
Lederer LG, Kidera GG (1954) Passenger comfort in commercial air travel with reference to
motion sickness. Int Med 167:661–668
Lindseth PD, Lindseth GN (1992) Assessing for pre-flight predictor of airsickness. Aviat Space
Environ Med 63:908–913
Littauer DI (1943) Service trials of therapeutic substances. National Research Council of Canada.
Minutes of the sixth meeting, sub-committee on motion sickness
Llano GA (1955) Airmen against the sea: an analysis of sea survival experiences. ADTIC
Publication G-104, Montgomery, AL, Research Studies Institute, Maxwell Air Force Base
Lucertini M, Lugli V, Casagrande M, Travelloni P (2008) Effects of airsickness in male and female
student pilots; adaptation rates and 4-year outcomes. Aviat Space Environ Med 79:677–684
McCauley ME, Royal JW, Wylie CD, O’Hanlon JF, Mackie RR (1976) Motion sickness
incidence: exploratory studies of habituation, pitch and roll, and the refinement of a
mathematical model. Technical report no. 1733-2, Human Factors Research, Incorporated,
Santa Barbara Research Park, Goleta, CA, April 1976
McDonough FE (1943) Committee on aviation medicine. Report no. 181, National Research
Council, July 1943
Money KE (1970) Motion sickness. Physiol Rev 50:1–38
Money KE (1991) Simulator sickness. In: Motion sickness: significance in aerospace operations
and prophylaxis. AGARD-LS-175. NATO/AGARD, Neuilly-sur-Seine. 6B, pp 1–4
Money KE, Myles WS (1975) Motion sickness and other vestibulo-gastric illnesses. In:
Naunton RF (ed) The vestibular system. Academic Press Inc., New York
Naval Medical Information Center (1996) Letter serial 42hg/0130-96, dated 30 July 1996
O’Hanlon JF, McCauley ME (1974) Motion sickness incidence as a function of the frequency of
acceleration of vertical sinusoidal motion. Aerosp Med 45(4):366–369
Oman CM, Lichtenberg BK, Money KE (1984) Space motion sickness monitoring experiment:
spacelab 1. In: Motion sickness: mechanisms, prediction, prevention and treatment. AGARD
conference proceedings no. 372, North Atlantic Treaty Organization Advisory Group for
aerospace research and development, Neuilly-sur-Seine, France, vol 35, pp 1–21
References
55
Park J (1943) Airsickness in gliders. British Flying Personnel Research Committee. Report no. 510
Perrin P, Lion A, Bosser G, Gauchard G, Meistelman C (2013) Motion sickness in rally car
co-drivers. Aviat Space Environ Med 84:473–477
Pethybridge RJ (1982) Sea sickness incidence in Royal Navy ships. INM Report 37/82, Institute of
Naval Medicine, Gosport
Reason JT (1967) Relationships between motion after-effects, motion sickness susceptibility and
receptivity. PhD thesis, University of Leicester
Reason JT, Brand JJ (1975) Motion sickness. Academic Press, New York
Reason JT, Diaz E (1971) Simulator sickness in passive observers. Ministry of Defence (Air Force
Department), Flying Personnel Research Committee, FPRC/1310
Regan EC, Price KR (1994) The frequency of occurrence and severity of side-effects of immersion
virtual reality. Aviat Space Environ Med 65:527–530
Rubin HJ (1942) Airsickness in a primary air force training detachment. J Aviat Med 13:272–276
Ryback RS, Rudd RE, Matz GJ, Jennings CL (1970) Motion sickness in USAF flying personnel.
Aerosp Med 41:672–677
Steele JE (1968) The symptomatology of motion sickness. In: NASA SP-187. Fourth symposium
on the role of the vestibular organs in space exploration, Naval Aerospace Medical Institute,
Pensacola, Florida
Strongin TS, Charlton SG (1991) Motion sickness in operational bomber crews. Aviat Space
Environ Med 62:57–59
Turner M, Griffin MJ (1995) Motion sickness incidence during a round-the-world yacht race.
Aviat Space Environ Med 66:849–856
Turner M, Griffin MJ (1999) Motion sickness in public road transport: passenger behaviour and
susceptibility. Ergonomics 42:444–461
Turner M, Griffin MJ, Holland I (2000) Airsickness and aircraft motion during short-haul flights.
Aviat Space Environ Med 71:11811189
Tyler DB (1946) Influence of placebo, body position and medication on motion sickness. Am J
Physiol 146:450–466
Tyler DB, Bard P (1949) Motion sickness. Physiol Rev 311–369
Walters JD (1964) Motion sickness. J Philippine Fed Private Med Pract 13:789–796
Wiker SF, Kennedy RS, McCauley ME, Pepper RL (1979a) Susceptibility to seasickness:
influence of hull design and steaming direction. Aviat Space Environ Med 50:1046–1051
Wiker SF, Kennedy RS, McCauley ME, Pepper RL (1979b) Reliability, validity and application of
an improved scale for assessment of motion sickness severity. USCG technical report no.
CG-D 29–79, U.S. Coast Guard Office of Research and Development, Washington DC
Witmer B, Lampton D (2000) Simulator sickness in virtual environments. Hum Syst IAC Gateway
XI(2):16–17
Chapter 3
Correlates of Susceptibility to Motion
Sickness
Abstract The incidence of motion sickness can be affected by a number of individual factors. In this chapter, I propose to introduce you to some of the personal
features that have been identified as having a bearing on the response to provocative
motion, namely: age; sex of the subject; race or culture; and physical fitness. Some
of these can have an impact on military personnel; as you will see, there are no hard
and fast rules. More work is needed to investigate these suggested correlates both to
confirm the relationship and better understand the underlying reason for these
associations to exist.
There are wide variations among different people in their response to provocative
motion, as has been pointed out earlier. A number of individual features have either
been identified or investigated as having a bearing on the incidence of motion
sickness. These are in addition to the fundamental physiological, psychological and
personality factors that are addressed elsewhere in this book. These correlates are
important in their own right in terms of better understanding and managing motion
sickness. Failure to recognise this fact can complicate and cause errors in the
experimental investigation of motion sickness. Tyler and Bard (1949) have pointed
out that these factors necessitate careful planning of experimental groups to avoid
misleading bias in the results.
3.1
Motion Sickness Related to Age
Tyler and Bard (1949) have reported that motion sickness varies with age.
Anecdotal evidence has suggested that human infants have a low susceptibility, but
that may be partly due to being transported in the supine position. Byrne (1912) has
explained why he believes infants in arms are rarely sick: “either because they are
not called upon to perform much in the way of acts of equilibration, or because of
the undeveloped condition of the mechanisms of equilibration.” Susceptibility
appears to be at its highest between 2 and 12 years of age, and Reason (1968) has
© Springer Nature Switzerland AG 2019
T. G. Dobie, Motion Sickness, Springer Series on Naval Architecture,
Marine Engineering, Shipbuilding and Shipping 6,
https://doi.org/10.1007/978-3-319-97493-4_3
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3 Correlates of Susceptibility to Motion Sickness
reported that a significant reduction then takes place between the ages of 12 and
21 years. The incidence of motion sickness continues to decline beyond that age
and has been reported to be very low in the elderly population.
Nieuwenhuijsen (1958) carried out a motion sickness study on a voyage from
New York to Rotterdam in which the passengers aboard the ocean liner S.
S. Maasdam were exposed to the tail of Hurricane Hazel after an initially calm
voyage. Over a period of some 12 h the vertical acceleration had increased from 1
to 4 m/s/s. During that time the number of cases of seasickness increased from 16
(4%) to 88 (22%). He reported a high incidence of seasickness among men in the
50-year old group but reasoned that this was perhaps associated with work, family
and social stress. He pointed out that women in that age group are in the climacteric
and “also exposed to more or less the same tensions as the men.” The lowest
incidence of seasickness had been found in the 60th year and older age group.
Byrne (1912) has also given an opinion on this matter. As you will see, he has
attributed such changes to disease or degeneration.
In Byrne’s words:
Old age is frequently immune for numerous reasons but more particularly because of the
rule that in advancing years there is a tendency to arteriosclerosis and to bilateral atrophy
and degeneration of the auditory nerve. Those suffering from chronic wasting diseases and
from continued excesses in alcohol also seem to have a relative immunity. Here the cause is
deterioration of the vestibulo-cerebellar mechanisms thereby they do not so readily respond
to labyrinthine stimulation and depression, or deterioration of the cerebral and medullary
centres whereby the labyrinthine irritation is less effective in evoking the phenomena of the
malady in their full severity.
This explanation is of itself very interesting because it has a bearing on other
apparent aspects of postural stability in the older population. Observed decrements
may be explained by underlying pathology rather than by passage of years, per se.
More recently, however, Cheung and Money (1992) have shown that squirrel
monkeys undergo no change in susceptibility to motion sickness with increasing
age. The squirrel monkeys were approximately four years old at the beginning of
the study and typically they live approximately 15 years. These researchers conducted a longitudinal study that lasted more than ten years. Cheung and Money
have suggested that it is perhaps not age that affects susceptibility to motion
sickness, “but rather the development of behavioural strategies for coping with
different types of motion.”
3.2
Motion Sickness Related to the Sex of the Subject
Reason and Brand (1975) have observed that women are apparently more susceptible to motion sickness than men; pointing out, however, that there is no
evidence that this significant sex difference is due either to sex-linked differences in
adaptability or receptivity—the two principal sources of interpersonal variation
within the neural mismatch hypothesis. Back in the 19th Century, ships’ doctors
3.2 Motion Sickness Related to the Sex of the Subject
59
had often noted that difference. Reason (1968) has reported that in a questionnaire
study among students, women declared a significantly higher incidence of motion
sickness than men of similar age and travel experience at all ages, that is, before and
after the age of twelve years.
Nieuwenhuijsen (1958) carried out a survey of 193 passengers who had crossed
the Atlantic Ocean by ship and found that the ratio of male to female susceptibility
to seasickness had been of the order of 2:3. Lawther and Griffin (1988) have carried
out a survey of over 20,000 passengers on ferries crossing the English Channel and
these reports indicated that the females were more susceptible to seasickness than
males. In their study, the ratio was 3:5 in terms of reported incidence of vomiting in
all age groups over 15 years. These responses indicate that this difference between
men and women in terms of the ratio of susceptibility to motion sickness, age for
age, is of the order of 1:1.7 which is very similar to Nieuwenhuijsen’s findings.
Kaplan (1964) had carried out a study of motion sickness on trains and noted
that females reported a greater susceptibility than males in the ratio of 327 females
to only 96 males, despite the fact that there had been a larger number of male
passengers. As part of a larger investigation on behavioural characteristics
involving undergraduate students, Lentz and Collins (1977) noted that more women
than men had reported susceptibility to motion sickness on a 20-item questionnaire.
During a study involving professional trainee pilots carried out by Lindseth and
Lindseth (1995), these researchers found that 75% (six out of a total of eight) of the
female pilots experienced airsickness, compared with only 20% (ten out of a total of
49) of their male counterparts.
In a simulator study, already discussed, Reason and Diaz (1971) observed that
on the basis of their Well-Being Ratings and their Symptom Scores, female subjects
had been considerably more affected by the car simulator than the male subjects.
Kennedy et al. (1995) also reported a higher incidence of simulator sickness in
females than in males.
It has already been stated that Davis et al. (1988) found no statistical difference
in terms of motion sickness in microgravity when they reported on 85 first-time
Shuttle crewmembers (77 males, 8 females). In view of the small number of females
in the sample, however, this matter requires further review when the numbers have
increased.
Benson (1988) has stated that the reason for this sex difference, which is
applicable to both children and adults, was not known. However, he has suggested
that perhaps females were more ready to admit to having had symptoms of motion
sickness. It might also have been that some males were less likely to admit their
susceptibility because of their wish to exhibit a macho image. Perhaps experience
also played a part, because males tended to exhibit a more “rough and tumble
lifestyle” which might have provided some protection against provocative motion.
On the other hand, repetitive exposure to provocative motion in automobiles has not
prevented some individuals from continuing to suffer from motion sickness, so the
question remains open.
My colleagues and I (Dobie et al. 2001) carried out a questionnaire study into the
effects of sex, age and physical activities on susceptibility to motion sickness in
60
3 Correlates of Susceptibility to Motion Sickness
order to examine some of these possible explanations. A total of 443 subjects,
ranging in age from 9 to 18 years took part in the study; of these 207 were female
and 236 male. Figure 3.1 shows the results from the subjects’ questionnaires related
to sex differences in terms of the amount of exposure on each of 13 types of
transport. This has revealed that there were a few sex differences in terms of the
exposure history of these various forms of transport. Males recorded more exposure
on trains, aeroplanes and small boats, whereas females had greater exposure to
merry-go-rounds, whereas in terms of the other forms of transport shown in Fig. 3.2
it can be seen that the differences in them, indicative of the difference between the
sexes is relatively small.
For those subjects who reported exposure to various forms of transport, their
motion sickness responses to these forms of transport are shown in Fig. 3.2. These
results indicate that, in general, males reported significantly less motion sickness
than females on provocative motion devices. Each subject’s motion sickness
response has been coded 0, 1, 2 or 3 for each device and the results for nausea/
queasiness showed that there were significant sex differences for automobiles,
buses, trains, airplanes, small boats and merry-go-rounds, whereby males reported
less nausea for each of these categories. These results are in general agreement with
Fig. 3.1 Mean exposure scores for females and males indicating the frequency of use on thirteen
modes of transport
3.2 Motion Sickness Related to the Sex of the Subject
61
Fig. 3.2 Mean motion sickness scores (vomiting) for females and males on each of thirteen
modes of transport
previous studies and provide specific support for the notion that females are more
susceptible to motion sickness.
In terms of vomiting, the reported incidence for the various forms of transport is
shown in Fig. 3.2. As might be expected, the incidence is quite low. Only one
significant sex difference is evident, namely that related to a lower incidence of
vomiting in automobiles reported by males. These results have revealed significantly greater motion sickness for female, when compared to male, subjects on
devices with which both groups have been equivalent in terms of their exposure
history.
In addition, our study has demonstrated little relationship between an individual’s level of physical activity and their susceptibility. In other words, we have not
been able to show any evidence of either habituation or sensitivity caused by an
individual’s participation in any of the 17 leisure and sporting activities that have
been surveyed in the questionnaire. There has also been little evidence to suggest
that males are more reticent than females to report motion sickness.
Some time later we carried out another experiment at UNO (Flanagan et al.
2005) to investigate sex differences in tolerance to visually-induced motion sickness. In the first experiment we used a motion sickness history questionnaire which
gave the male and female participants the option to volunteer for physiological
62
3 Correlates of Susceptibility to Motion Sickness
experiments and also used the data to determine the effects of sex and volunteer
status on their susceptibility to motion sickness. In the second experiment the
volunteers were exposed to rotation of a Dichgans and Brandt type of drum (see
Fig. 13.2), striped on the inside under static and head movement conditions. The
findings of the first experiment agreed with previous publications that women were
more prone to motion sickness than men. It was also clear from the second
experiment that, although there weren’t any differences between vection measures
across the sexes, or head movement conditions, females were more susceptible than
men. So it does seem to be quite clear that females really are more susceptible to
motion sickness than males, but why should this be so? We were unable to go
further with this question in our study, so let us see what is in the literature.
3.3
Why Are Females More Likely to Be Motion Sick?
Reason and Brand (1975) believed that certain factors could be excluded in terms of
explaining this sex difference. For example, they were of the opinion that there was
no reason to believe that females showed a greater sensory response to the nauseogenic features of provocative motion. They also stated that there was no
apparent evidence that their ability to adapt was any different from that of men.
Schwab (1954) pointed out that in the adult female, hormonal factors might be
implicated since susceptibility to motion sickness has been reported to be highest
during menstruation and increased in pregnancy. On the other hand, Reason (1968)
has found, as stated above, that there was a difference between males and females
even before the age of twelve years. So this question awaits further study of these
different possibilities.
During their extensive study of the occurrence of sickness during the 1992–1993
British Steel Challenge 9 months round-the-world yacht race, Turner and Griffin
(1995) have examined various individual factors. For example, during the 2-year
training period and all four legs of the race, they had not found any significant
differences in the incidence of seasickness between males and females. However,
they found that females reported seasickness on a greater percentage of days than
males (females: mean of 7.0%; males: mean of 3.6%). In addition, the females
reported a significantly greater amount of vomiting than males in terms of the
number of days during which they had vomited (2.9 and 1.1%, respectively).
Grunfeld et al. (1998) carried out a questionnaire study of motion sickness
during the 1997 British Telecom yacht race (“Global Challenge”) that consisted of
six legs varying from 8 to 45 days. Many of the sailors had become seasick at some
time during the race. Daily logs were kept by 25 men and 27 women in which they
recorded any headache or symptoms of seasickness, and the women had taken
additional notes of the dates of their menstrual periods. Female crewmembers were
found to be most susceptible to seasickness from 3 days before the onset of
menstruation to the fifth day after. Headache has also been at its greatest during that
same time period. On the other hand they reported that the incidence of seasickness
3.3 Why Are Females More Likely to Be Motion Sick?
63
was at its lowest around the time of ovulation, but again headache peaked at that
time. These results lend credence to the idea of a possible link between motion
sickness and hormonal changes. However, this is another matter that requires further investigation in order to validate this concept and to identify the particular
hormonal factors that are implicated.
3.4
Motion Sickness Related to Race or Culture
Stern et al. (1993) reported a chance observation from their laboratory that most
Chinese subjects became motion sick when exposed to experimental provocative
motion. Stern and his colleagues then specifically investigated this matter by
comparing the gastric responses and reports of motion sickness symptoms of
Chinese subjects during optokinetic stimulation with those obtained from healthy
female college students and they did so by dividing the subject population into three
groups.
There were 15 subjects in each group, as follows: Chinese who were born in
China, European-Americans born in the United States, and African-American
subjects also born in the United States. There had been no significant difference in
the responses to visually-induced apparent motion of European-American and
African-American subjects. However, the Chinese subjects had shown significantly
greater disturbances in terms of their gastric activity, as recorded by electrogastrography, and they also reported a significantly greater degree of motion sickness.
Stern and his co-workers had no definitive explanation for these results but suggested that this higher level of susceptibility to provocative motion provided an
interesting natural model for studying the physiological mechanisms underlying the
causation of nausea and other symptoms of motion sickness.
3.5
Motion Sickness Related to Physical Fitness
Parnell and Whinnery (1982) have first reported an increase in susceptibility to
motion sickness induced by aerobic training. When they investigated the relationship of aerobic fitness to ±Gz tolerance, they observed a significant number of
symptoms of motion sickness among those subjects who were aerobically fit. These
results have not yet been explained, however. Some five years later Banta et al.
(1987) decided to compare the signs and symptoms of motion sickness induced by
cross-coupled (Coriolis) stimulation among groups of subjects with different levels
of aerobic fitness. Their subject population was drawn from people who were
non-smokers, non-obese (less than 20% body fat), and who had reported neither
recent nor routine exposure to disorienting manoeuvres. The history of each subject’s aerobic exercise regimen was then evaluated and a subject pool of 29 males
has been selected.
64
3 Correlates of Susceptibility to Motion Sickness
This population was sub-divided into the following 3 groups having: high
(extreme exercise three to four times per week, for more than 30 min duration),
moderate (routine exercise two to three times per week, between 20 and 30 min
duration), and low levels of aerobic fitness (no routine exercise programme). The
subjects’ final fitness classification was made by means of aerobic fitness analysis,
based on laboratory tests. The subjects then underwent cross-coupled (Coriolis)
vestibular stimulation on a Stille-Werner rotating chair during a ten-minute modification of the Brief Vestibular Disorientation Test (BVDT). This test is described
later in Chap. 8. A number of variables were evaluated, namely: duration of rotation
before aborting, heart rate, respiratory rate, mean skin temperature, subject observation values and observed values.
Banta et al. found that significant differences in the duration of rotation existed
only between the high and low aerobic groups, with the high aerobic group
demonstrating a shorter spinning time and greater self-rated sickness values than the
low aerobic group. In terms of the total population, they found that aerobic fitness
and the duration of rotation before aborting were inversely related. Only limited
differences in heart and respiration rates and mean skin temperatures between
groups were revealed during spinning. Regarding skin temperature at the thigh and
calf, analysis has shown a significant decrease from pre-to-post spinning across all
groups resulting in a change in the mean skin temperature.
There has been, however, no temperature change between the groups. These
researchers postulated that the small decrease in temperature was perhaps environmental and could be accounted for by the passage of air across the subjects’
lower limbs while they were spinning. They did not consider that any of the
physiological responses that they had reported were due to motion sickness. In all 3
groups, the subject heart rates have been higher at the beginning of spinning,
compared to the resting situation, but in their opinion this simply indicated minor
anticipatory anxiety. So, based upon these data, Banta et al. agreed with the
observations of Parnell and Whinnery that men who had exhibited a high aerobic
fitness level appeared to be more susceptible to motion sickness than others.
In that same year, Whinnery and Parnell (1987) published their findings on
aerobic conditioning, which they had presented to the Annual meeting of the
Aerospace Medical Association (Parnell and Whinnery 1982). During these studies,
which had been carried out at the USAF School of Aviation Medicine (USAFSAM)
during medical evaluation on a human centrifuge, they had found that 52% of those
subjects who were aerobically conditioned through endurance training complained
of symptoms of motion sickness and 38% of that group progressed to vomiting.
These numbers were then compared with data relating to the medical evaluation of
subjects from the whole USAFSAM human centrifuge data repository, for the same
three-year period, and found that the incidence of motion sickness was much lower.
The incidence of motion sickness in the latter overall group had been only 23%,
with a 7% incidence of vomiting. Whinnery and Parnell suggested that the
increased incidence of motion sickness might have resulted from the increase in
vagal tone, which has been associated with intense aerobic training. They also
pointed out that the duration of spinning during brief vestibular stimulation tests
3.5 Motion Sickness Related to Physical Fitness
65
was shorter for those subjects who were highly conditioned and drew attention to
the significance of these observations in terms of defining optimal conditioning
programmes for aviators and the like.
Jennings et al. (1988) pointed out that several investigators had already linked
aerobic fitness with motion sickness sensitivity in the 1-G or high-G environment.
In their own study, however, they have investigated the relationship of aerobic
fitness of 125 Shuttle crewmembers with the severity or absence of space motion
sickness, in conditions of microgravity. The categories of susceptibility to motion
sickness that they used have already been described in Table 2.3, in the previous
chapter. This is another example of evaluating not only the symptoms of motion
sickness but also the effect of this malady on performance, which is clearly a very
important factor.
Astronauts routinely undergo an annual exercise tolerance test, and aerobic fitness measures are obtained from the nearest exercise tolerance test information to
the time of launch; this is usually within six months of the flight. The space motion
sickness data obtained from the post-flight medical debriefing summaries were then
compared with the mean maximum oxygen consumption (V̇O2 max) for four categories of crewmembers, as follows: namely, no motion sickness, mild, moderate or
severe motion sickness. The associated values for (V̇O2 max) were 44.55, 44.08,
46.50, and 44.24 ml/kg/min, respectively, and the correlation coefficients for both
men and women showed no significant relationship between space motion sickness
and aerobic fitness. In view of the subjective nature of the data, however, they
recommended that further studies be carried out to elucidate these findings.
Jennings et al. concluded that while there might be a correlation between aerobic
fitness and susceptibility to motion sickness in the high-G or 1-G motion environments, their preliminary findings have suggested that there is no such relationship in a microgravity environment. They also recommended that it might be
better to use the resting pulse rate recorded on the day before launch as the measure
of aerobic fitness, rather than maximum oxygen consumption measured some time
before that.
Cheung et al. (1990) reviewed the experimental designs utilised by Whinnery
and Parnell (1987) and Banta et al. (1987) and were of the opinion that it was
difficult to be confident that they could demonstrate a causal relationship between
aerobic fitness and susceptibility to motion sickness. For their part, therefore,
Cheung et al. decided to carry out a longitudinal study to re-examine the susceptibility to motion sickness of subjects who were initially unfit, before and after they
have undergone a programme of endurance training. Provocative motion was
provided by means of a Precision Angular Mover®, which is a rotary device that
can provide rotation about the Earth-horizontal axis. The subject underwent tumbling, head over heels in darkness, about that axis, at a rate of 20 cycles per minute.
Previous studies on the device have shown this axis of rotation to be more
provocative than either roll or yaw. Bicycle ergometry was used to measure
maximal aerobic power and the blood lactate response to submaximal exercise. The
researchers found that this form of physical training has created both a significant
improvement in (V̇O2 max) endurance capacity as well as a significant increase in
66
3 Correlates of Susceptibility to Motion Sickness
susceptibility to motion sickness. These results have indicated that in some individuals at least, an increase in their physical fitness has made them more susceptible
to motion sickness. Cheung et al. were of the opinion that their results suggested
that the relationship between an individual’s adrenocorticotrophic hormone levels
and both their susceptibility to motion sickness and aerobic fitness bear closer
study.
Rowat et al. (2002) have also carried out a study to investigate the correlation
between aerobic fitness and susceptibility to motion sickness in a group of seven
male and two female volunteers ranging in age from 20 to 38 years, and with a
variety of exercise histories. They induced provocative motion with a Bárány chair
and measured aerobic fitness by means of V̇O2 max using the Leger test as a
method of predicting oxygen consumption. They concluded that their study did
suggest a relationship between susceptibility to motion sickness and aerobic fitness.
However, they also noted that aerobic capacity “is more specifically linked to signs
and symptoms of vasomotor origin including stomach discomfort, nausea and/or
vomiting, headache and diaphoresis.” As they have concluded, alterations in vagal
activity seemed to account for this relationship between aerobic fitness and susceptibility to motion sickness, but that further studies were needed to confirm this.
The relationship of the incidence of motion sickness to a subject’s state of fitness
raises the interesting question of the implication of endorphins in this matter. These
are neuropeptides which, like opiates, have the ability to reduce pain. So the body
could, in a sense, generate its own “painkillers” and this might occur during heavy
exercise. Naloxone is a narcotic antagonist that prevents or reverses the effects of
opioids. Using a double-blind crossover protocol, Allen et al. (1986) investigated
the actions of naloxone and the role of endogenous opiates on the mechanisms
involved in the control of nausea and vomiting caused by exposure to cross-coupled
(Coriolis) stimulation induced by active head movements on a rotating chair. They
measured the time course to Malaise III in human subjects who have been given
either naloxone or a placebo. They found that subjects reached their Malaise III
level of motion sickness sooner after the naloxone injection, than with the placebo
and, unlike with the placebo, their discomfort continued for up to three days.
Allen et al. have suggested that endogenous opiates are elevated during exposure
to provocative motion and have presumed that the unblocked endorphins would
have the effect of inhibiting the motion sickness response. They have also suggested
that when subjects experienced the withdrawal of endogenous opioids, such as after
heavy exercise, they could be more sensitive to exogenous emetic stimuli due to
hypersensitivity. As a consequence, they have postulated greater tolerance to
provocative motion in subjects whose endorphins had been raised repeatedly by
avoiding a state of hypersensitivity from endogenous opiate withdrawal. These
authors further stated that since acupuncture or transepidermal nerve stimulation
could elevate endorphins, these techniques might prove to be beneficial in reducing
motion sickness.
Perhaps these individual differences in response to provocative motion reflect a
particular individual’s position along the underlying causative psycho-physiological
spectrum, which can vary from person to person and stimulus to stimulus, with
3.5 Motion Sickness Related to Physical Fitness
67
differing personal attitudes and amounts of associated arousal. For example, sport
fishermen commonly report that: “when the fish are biting, I don’t get sick!” This
question will be addressed further toward the end of Chap. 6, when I discuss
various psychological mechanisms that exacerbate motion sickness.
3.6
Summary
• It has been suggested that motion sickness varies with age, but this is not
absolutely clear-cut. Others have suggested that age, per se, is not what affects
motion sickness, but the development of behavioural strategies for coping with
different types of motion.
• Age for age, women appear to be more susceptible to motion sickness than men.
• Recent evidence suggests that this difference in susceptibility between the sexes
may have a hormonal origin.
• Some say that individuals who are aerobically fit show a significant number of
symptoms related to motion sickness, but others have disputed this.
References
Allen ME, McKay C, Eaves DM, Hamilton D (1986) Naloxone enhances motion sickness:
endorphins implicated. Aviat Space Environ Med 57:647–653
Banta GR, Ridley WC, McHugh J, Grissett JD, Guedry FE (1987) Aerobic fitness and
susceptibility to motion sickness. Aviat Space Environ Med 58:105–108
Benson AJ (1988) Motion sickness. In: Ernsting J, King P (eds) Aviation medicine, 2nd edn.
Butterworth-Heinemann Ltd., Oxford
Byrne J (1912) On the physiology of the semicircular canals and their relation to seasickness. J. T.
Dougherty, New York
Cheung BSK, Money KE (1992) The influence of age on susceptibility to motion sickness.
Aviation Space Environ Med 63:38 (abstract)
Cheung BSK, Money KE, Jacobs I (1990) Motion sickness susceptibility and aerobic fitness: a
longitudinal study. Aviat Space Environ Med 61:201–204
Davis JR, Vanderploeg JM, Santy PA, Jennings RT, Stewart DF (1988) Space motion sickness
during 24 flights of the space shuttle. Aviat Space Environ Med 59:1185–1189
Dobie TG, McBride D, Dobie TG Jr, May JG (2001) The effects of age and sex on susceptibility to
motion sickness. Aviat Space Environ Med 72:13–20
Flanagan MB, May JG, Dobie TG (2005) Sex differences in tolerance to visually-induced motion
sickness. Aviation Space Environ Med 76:642–646
Grunfeld EA, Price C, Goadsby PJ, Gresty MA (1998) Motion sickness, migraine, and
menstruation in mariners. Lancet 3511:1106
Jennings RT, Davis JR, Santy PA (1988) Comparison of aerobic fitness and space motion sickness
during the shuttle program. Aviat Space Environ Med 59:448–451
Kaplan I (1964) Motion sickness on railroads. Ind Med Surg 33(1):648–651
Kennedy RS, Lanham DS, Massey CJ, Drexler JM, Lilienthal MG (1995) Gender differences in
simulator sickness incidence: implications for military virtual reality systems. SAFE J 25
(1):69–76
68
3 Correlates of Susceptibility to Motion Sickness
Lawther A, Griffin MJ (1988) A survey of the occurrence of motion sickness amongst passengers
at sea. Aviat Space Environ Med 59:399–406
Lentz JM, Collins WE (1977) Motion sickness susceptibility and related behavioral characteristics
in men and women. Aviat Space Environ Med 48:316–322
Lindseth G, Lindseth PD (1995) The relationship of diet to airsickness. Aviat Space Environ Med
66:537–541
Nieuwenhuijsen JH (1958) Experimental investigations on seasickness. Ph.D. thesis, University of
Utrecht, The Netherlands
Parnell MJ, Whinnery JE (1982) The effects of long term aerobic conditioning on tolerance to +Gz
stress. In: Paper presented at the aerospace medical association annual scientific meeting,
Washington, DC, pp 22–23 (preprint)
Reason JT (1968) Relations between motion sickness susceptibility, the spiral aftereffect and
loudness estimation. Br J Psychol 59:385
Reason JT, Brand JJ (1975) Motion sickness. Academic Press, New York, NY
Reason JT, Diaz E (1971) Simulator sickness in passive observers. Ministry of Defence (Air Force
Department), Flying Personnel Research Committee, FPRC/1310
Rowat N, Connor CW, Jones JA, Kozlovskaya IB, Sullivan P (2002) The correlation between
aerobic fitness and motion sickness susceptibility. Aviat Space Environ Med 73:216–218
Schwab RS (1954) The nonlabyrinthine causes of motion sickness. Int Record Med General Pract
Clin 167(12):631–637
Stern RM, Hu S, Koch KL (1993) Chinese hypersusceptibility to vection-induced motion sickness.
Aviat Space Environ Med 64:827–830
Turner M, Griffin MJ (1995) Motion sickness incidence during a round-the-world yacht race.
Aviat Space Environ Med 66:849–856
Tyler DB, Bard P (1949) Motion sickness. Physiol Rev 311–369
Whinnery JE, Parnell MJ (1987) The effects of long-term aerobic conditioning on +Gz tolerance.
Aviat Space Environ Med 58:199
Chapter 4
Characteristics of the Provocative
Motion Stimuli
Abstract A considerable amount of work has been performed in an attempt to
identify the characteristics of motion that provoke motion sickness. As you will see,
this has ranged from studies in the laboratory to others that have taken place in
environments more akin to the real world. Apart from giving us a better understanding of the mechanism of motion sickness, these data provide valuable design
criteria to reduce provocative vehicular responses; in addition, however, we must
not forget the operator’s personality and cognition. This is an example of the value
of recognising the need to design with the human operator or traveller in mind from
day one.
In attempting to discover the causes of the symptoms and signs of motion sickness
and their physiological origins, numerous investigators have tried to reproduce
these responses by means of artificial stimulation. Tyler and Bard (1949) reported
that there have been four basic approaches to investigating motion sickness
experimentally. These were the use of swings, rotating-tilting chairs, elevators and
more complex devices built to simulate ship motion. For example, Noble (1945)
reported the effect of provocative motion on dogs susceptible to motion sickness,
using the three components of swing motion, namely, vertical, horizontal and
angular. The composite motion has been shown to be more provocative than any
one of the single components.
In human subjects, McIntyre (as cited by Tyler and Bard) confirmed the belief
that the repetition of a combination of accelerations in different planes created a
more potent provocative stimulus than the mere repetition of any one of these
accelerations alone. It has been reported that movements that cause large accelerations with short pauses are less provocative than those that cause small accelerations with long pauses. In a series of studies carried out at Wesleyan University,
Wendt and his colleagues (Alexander et al. 1945a, b, c, d) decided to examine this
observation further by using a “wave machine,” similar to an elevator, in order to
study the time intervals between accelerations and their results have confirmed
these findings. So, as a result of this, these investigators have concluded that the
© Springer Nature Switzerland AG 2019
T. G. Dobie, Motion Sickness, Springer Series on Naval Architecture,
Marine Engineering, Shipbuilding and Shipping 6,
https://doi.org/10.1007/978-3-319-97493-4_4
69
70
4 Characteristics of the Provocative Motion Stimuli
total energy per wave was more potent, in terms of being able to provoke motion
sickness, than the actual interval between these accelerations.
However, as already pointed out (Reason and Brand 1975) motion sickness can
be caused by purely visual stimulation, without any associated bodily accelerations,
as well as by motion that causes changing linear and angular accelerations. They are
characterised by the presence of visual information indicating whole-body motion
in the absence of corroboration from the inertial receptors. In other words motion
sickness occurs where the vestibular stimulation that is expected to accompany the
motion that has been seen is missing.
4.1
Laboratory Studies
Allen (1974) has stated “mechanical vibration is a pervasive environmental stress,
causing undesirable reactions ranging from discomfort and impaired efficiency to
pain and injury.” He pointed out that in ships and other forms of transport, there
was a considerable amount of low frequency energy below 1 Hz that can cause
motion sickness. Allen also noted that much of the literature was related to the
effects of vertical motion. This is partly because some, but not all as we shall see,
believe that it is the critical component in this context, but also because there is a
lack of data concerning other modes. In terms of ride comfort he has described,
“initial proposals for limiting vertical vibration for 0.1–1.0 Hz for seated and
standing adults and durations of 25 min and 8 h have been made.” However, Allen
then stressed the point that considerably more effort would be needed to investigate
the human responses to very low frequency vibration.
Morton et al. (1947) reviewed a series of studies carried out by researchers in
Montreal, Canada during World War II to investigate the mechanisms underlying
motion sickness. For this purpose, they designed and built a “Roll-Pitch Rocker” to
simulate ship motion at sea. It consisted of a giant rocker that rolled from side to
side. On top of the rocker was a counter-weighted seesaw, at one end of which the
subject was seated; the seesaw moved up and down like a ship pitching. These two
motions could be used separately or together, at various speeds. The roll component
has extended over 26.5° and the pitch a total of 3.6 m (12 ft). They also used two
electromechanically driven swings with a maximum radius of 4.3 m (14 ft), a
period of 15 Hz and a total arc of 90°. This machine reproduced the movements of
a ship in a very realistic way. The incidence of motion sickness induced by this
experimental device can be found in Chap. 1, Table 1.2. In addition, they used
hand-operated swings to study motion effects on animals.
They described an unexpected inconsistency in the incidence of motion sickness
as a result of relatively minor alterations in the motion profiles. Pitching motion
alone was as provocative as the combination of pitch and roll and to some extent
there has been an increase in the incidence of sickness as the frequency of pitching
increases. Five subjects were exposed to pure vertical motion on an elevator over a
4.1 Laboratory Studies
71
range of 5 m with an acceleration of about 0.275 g at a maximum speed of 4 m per
second. Four of these subjects became sick after some 10–30 min.
Morton et al. found that although both simulated ship motion on their
“Roll-Pitch Rocker” and simple pendulum swings have produced motion sickness,
some individuals who had been susceptible to one form of motion had not been
affected by the other. I have had similar experiences recently when comparing
responses to Coriolis stimulation and illusory motion. Morton et al. concluded that
vertical acceleration and deceleration in the long axis of the body, head erect,
seemed to produce the greatest amount of motion sickness which led them to
suggest that the most important aetiological factor is “stimulation of the utricles by
linear accelerations in the vertical plane of the head.”
Johnson and Taylor (1961) investigated the effectiveness of riding on a 2-pole
and a 4-pole swing as a means of causing motion sickness when the subject’s head
has been either free or fixed to the swing, as well as with or without visual stimuli.
Their 2-pole swing possessed the characteristics that Noble (1945) had found to be
most provocative in terms of causing motion sickness. The radius was 15 ft; the
swinging frequency was 16 cycles per minute and the arc was 70°. This type of
swing provided simple harmonic motion; and the acceleration was proportional to
the displacement from the mid-position, in one plane. In the 2-pole configuration,
the acceleration of the subject’s chair could be resolved into horizontal, vertical and
angular components. The swing was then converted into a 4-pole version in which
the acceleration could only be resolved into horizontal and vertical components,
since there was no angular motion without rotation.
Johnson and Taylor found that the highest incidence of motion sickness was on
the 2-pole swing when the subject’s eyes were closed and the head was free to
move. The next highest incidence was on the 4-pole swing under the same subjective conditions (Table 4.1). They deduced that motion sickness was mainly
induced by angular accelerations due to head movements. They drew attention to
Table 4.1 Incidence of motion sickness on 2-pole and 4-pole swings
Swing condition
Motion sick (%)
Head free, eyes closed
2-pole
35
4-pole
20
Head fixed, eyes closed
2-pole
5
4-pole
7
Head free, eyes open
2-pole
2
4-pole
4
Head fixed, eyes open
2-pole
7
4-pole
3
Not sick (%)
Total number of subjects (n = 800)
65
80
218
50
95
93
200
128
98
97
46
57
93
97
43
58
72
4 Characteristics of the Provocative Motion Stimuli
the fact that on the 2-pole swing there has been a marked reduction in the incidence
of motion sickness when the subject’s head was restrained.
They interpreted the apparent protection afforded by having the eyes open as
perhaps indicating that the visual reference point might have assisted in the
reduction of head movements. Overall, they stressed that the accelerations considered to apply to various devices referred to the apparatus and not to the subject’s
head. If conclusions were to be reached regarding the effects of these accelerations,
it was essential to ensure that the subject’s head conformed, as far as possible, to
those of the equipment. Although there is a typographical error in Table 4.1 related
to the 4-pole swing data (head free, eyes open) it does not materially affect the
researchers’ conclusions, as stated:
In general, it has been possible to produce motion sickness under all conditions in which
angular accelerations of the head are present, and with angular accelerations alone (especially when in two planes), but difficult to effect with any degree of reliability under
conditions in which the head is exposed to linear acceleration, while the angular accelerations are reduced to a minimum. Linear acceleration, bad odours, previously existing
nausea or disease may affect the incidence of motion sickness but these are considered to be
secondary factors.
Lawther and Griffin (1986) pointed out that it was generally recognised that
particular characteristics of the motion of ships caused seasickness, but the precise
relationship was still not clear. A large programme of research involving surveys of
motion and sickness amongst passengers on ferries was undertasken. The initial
study, previously reported by Lawther and Griffin (1986) was carried out on a
4,000 tonne car ferry M. V. Earl Godwin. Motion was recorded in all six axes
throughout each voyage and a motion sickness questionnaire was administered to
passengers towards the end of each voyage. The survey involved 4,915 passengers
on 17 voyages of up to 6-h duration.
In general, the laboratory experiments have mostly involved sinusoidal stimulation and this has often been at high magnitudes so that it produced motion
sickness fairly quickly and commonly only involved a small number of subjects.
Whereas shipboard surveys have included many more subjects, usually over longer
periods of time; the methods used to measure ship motion and the associated
analyses have not always been very satisfactory.
As stated previously, these early laboratory studies of motion sickness mostly
used large swings but, as Lawther and Griffin have pointed out, there have been
many problems with non-uniformity of the waveform and confusing motion patterns in different axes, despite the size of the subject populations. Consequently,
they concluded that it was difficult to draw succinct conclusions from these studies
because of inadequate control over the experimental conditions and incomplete
reporting. The studies have shown, however, that in persons seated in the z-axis
(see Table 4.2) motion sickness could be produced by vertical motion with a frequency content below about 0.5 Hz. The combined data have further suggested that
at frequencies below about 0.3 Hz, a magnitude of acceleration around 0.5 m/s/s r.
m.s would cause vomiting in roughly 10% of unadapted persons over a period of
two hours.
4.1 Laboratory Studies
73
Table 4.2 Inertial response to forces of acceleration exerted upon the body
Direction of inertial forces on
the human body
Codified physiological
terminology (in G)
Current US/UK
“professional terminology”
From rear surface of body
towards front
From front towards rear
surface of body
From head towards feet
From feet towards head
From right side towards left
From left side towards right
+Gx
Eye balls in
−Gx
Eye balls out
+Gz
−Gz
+Gy
−Gy
Eye
Eye
Eye
Eye
balls
balls
balls
balls
down
up
left
right
More recently, it has been reported that subjects with normal vestibular function
could be made motion sick when exposed to visually-induced apparent (illusory)
motion while experiencing rotation in an optokinetic drum in the subject’s yaw axis
(Stern et al. 1989, 1993; Dobie et al. 1987). In view of these reports, Cheung et al.
(1991) have studied visually-induced motion sickness in groups of subjects with
normal vestibular function and others who were bilaterally labyrinthine defective.
They exposed nine normal subjects and six labyrinthine-defective subjects to a
visual field rotating about an Earth-horizontal axis (orthogonal to the gravity axis).
Rotating a 3 m-diameter sphere lined with random dots at 30°, 45°, 60° per second
around the stationary subject has produced the visual stimulation in the roll, pitch,
and yaw axes. The subject was positioned so that the head has been at the center of
the sphere, and has experienced visually-induced apparent motion in all three axes.
In the group with normal vestibular function, symptoms of motion sickness were
reported in 21 of the 27 trials. When labyrinthine-defective subjects experienced
roll and pitch stimulation, there were neither reports nor signs of motion sickness.
These workers concluded that their results provided strong evidence for the
necessity of an intact vestibular system in order to produce visually-induced motion
sickness.
Golding et al. (1995) theorised that the ability of low frequency linear oscillatory
motion to cause motion sickness depended upon the direction of motion with
respect to that of gravity, the orientation of the axis of the body in relation to the
direction of motion, and body posture. In order to test this hypothesis, they planned
two studies involving the following three experimental conditions, namely: seated
upright, horizontal motion, X-axis, (condition A); seated upright, vertical motion,
Z-axis, (condition B); and, supine, vertical motion, X-axis, (condition C). In the first
experiment, with the subject seated upright, they compared the likelihood of provoking motion sickness in 28 subjects exposed to low frequency linear oscillatory
motion in both the horizontal (condition A) and vertical (condition B) directions. In
the second experiment they repeated these conditions using 12 subjects and have
added a new condition (C), in which the subjects were exposed to vertical motion in
the supine position. In all conditions, the sinusoidal motion had the following
characteristics, namely: a frequency of 0.35 Hz and a peak intensity 3.6 ms−2. Each
74
4 Characteristics of the Provocative Motion Stimuli
subject has recorded a motion sickness rating every minute on a four-point scale, as
follows: (1 = no symptoms; 2 = mild symptoms without nausea; 3 = mild nausea
plus additional symptoms; 4 = moderate nausea plus other symptoms). Motion
stopped at sickness rating 4, or after 30 min if that severity level had not been
reached. Subjects were then asked to complete a symptomatology checklist
(dizziness, bodily warmth, headache, sweating, stomach awareness, increasing
salivation, nausea, and any other symptom) and rate the severity of their subjective
reactions on a four-point scale (0 = none; 1 = mild; 2 = moderate, 3 = severe). The
symptomatology score was the sum of these ratings. This is similar to the system
my colleagues and I had used in 1989, except that we subtracted any existing
symptomatology scores that had been recorded before a session from scores
obtained after a session in order to yield a change score.
Golding et al. found that horizontal motion provoked nausea twice as often as
vertical motion, but found no such difference between upright and supine postures
during exposure to vertical motion. In the first experiment, the mean durations of
motion exposure to achieve moderate nausea in the three experimental conditions
already described, were (A) = 9.0 and (B) = 22.4 min; and in the second experiment, (A) = 15.3, (B) = 27.1, and (C) = 22.5 min. Taking these results together
with those of a previous experiment (Golding and Kerguelen 1992), Golding et al.
(1995) have suggested that an upright posture and stimulation through the X-axis
both increased the nauseogenicity of low frequency linear oscillation, and that these
effects were additive. They further concluded, however, that the direction of motion
with respect to the gravity vector was less important.
In the following year, (Golding and Markey 1996) investigated the nauseogenic
response of linear oscillatory motion challenges in the horizontal direction, at the
following frequencies: 0.205, 0.350 and 0.500 Hz. They tested 7 healthy male and
5 healthy female subjects, age 18–47 years, all of whom had intact vestibular
function, and were not taking any medication. The subjects have all been considered representative of the normal population in terms of motion sickness susceptibility based on their Reason and Brand (1975) Motion Sickness Susceptibility
Questionnaire scores. The subjects were positioned, within an enclosed cab, on a
seat fitted with a headrest. Golding and Markey found that subjects seated upright
and exposed to horizontal motion experienced more nausea that would have been
predicted by the mathematical models that have been based on the data from
vertical oscillatory motion. They also found that the relationship of frequency to
severity of nausea was significantly less steep than that which had been found for
vertical motion.
Golding et al. (1997) then extended the frequency range of that 1996 study as
follows: 0.35, 0.50, 0.70 and 1.00 Hz. The first two frequencies were chosen to
overlap those of the previous year’s experiment and the newly added frequencies
extended the range upwards and might have been expected to show a rapid
diminution of nauseogenicity, based on previous data for vertical motion. The
subjects were in the same age range as before and similarly fit. But in terms of
motion susceptibility, this group of subjects was slightly less susceptible than those
in the previous study. Golding et al. found that their results had indeed confirmed
4.1 Laboratory Studies
75
and extended to those frequencies that were higher than those in their previous
study; horizontal translational oscillatory motion at frequencies above 0.5 Hz was
significantly less provocative in terms of nauseogenicity.
Golding et al. (2001) also carried out a further study of low frequency horizontal
translational oscillation in order to test their hypothesis that “nauseogenicity should
be maximal around 0.2 Hz.” They tested 6 male and 6 female healthy volunteers,
aged between 20 and 43 years, selected for their high susceptibility to provocative
motion. The subjects were required to rate their motion sickness responses every
minute on a 4-point scale, ranging from 1: no symptoms through 4: moderate
nausea. The motion challenge was restricted to a maximum response of level 4 on
that scale, or 30 min if that level had not been reached; the subjects also indicated
their recovery responses on that same scale. The horizontal motion was imposed in
a car that had been fitted with a cabin with enclosed seat and headrest, such that
visual and tactile cues were excluded. The subjects carried out a visual scanning
task throughout the procedure, in order to control attention and potentiate motion
sickness. The three experimental motion frequencies that have been used were 0.1,
0.2 and 0.4 Hz, with a peak acceleration of 1.0 m/s/s.
These workers found that for horizontal translational oscillatory motion acting
through the x-axis of the body and head, motion sickness nauseogenicity was at its
height around 0.2 Hz. In addition they found that this severity of response had
decreased significantly both above and below that level. In addition, the mean time
to reach the subjects’ motion endpoint was also shorter at that critical frequency
(11.2 min), whereas it had been 18 min at 0.1 Hz and 20.2 min at 0.4 Hz. Golding
et al. have therefore concluded that they had shown to have substantiated their
original prediction that there has been a maximal nauseogenicity response to horizontal translational oscillation around the frequency of 0.2 Hz.
Griffin and Mills (2002a) further studied the effect of frequency and direction of
horizontal oscillation on the motion sickness response. In this case, they have
chosen to examine the frequency of oscillation over the range 0.2–0.8 Hz, in both
fore-and-aft and lateral directions, using the severity of motion more appropriate to
that found in public transport. They selected at random, 192 male subjects, aged
18-25 years, who were then randomly assigned to one of 16 groups, so that there
were no significant differences in terms of age, motion sickness susceptibility,
frequency of travel or associated motion responses. Griffin and Mills found that in
terms of horizontal sinusoidal oscillations that had the same peak velocity, the
average illness ratings across the seven chosen frequencies of oscillation from 0.2–
0.8 Hz, were slight. Each end of the frequency range produced approximately the
same potential for mild nausea, whereas, the risk was increased in the middle of the
range (0.315–0.400 Hz). There were no significant differences between the two
directions of oscillation. Griffin and Mills concluded that the motion sickness
response to horizontal oscillation roughly depended upon the velocity of motion,
bearing in mind the complex frequency weighting reflecting the lower responses
reported at each end of the frequency range.
Griffin and Mills (2002b) pointed out that motion sickness in land transport was
commonly associated with vertical and horizontal oscillation. In which case, they
76
4 Characteristics of the Provocative Motion Stimuli
opined that an increased magnitude and/or duration of exposure would increase any
of the following: the number of people affected; the severity and number of
symptoms; or would provoke an earlier onset of the symptoms. They carried out a
series of experiments with 144 male subjects, aged 18–25 years, using a frequency
of 0.315 Hz horizontal oscillation, in a closed cabin, for 30 min with eyes open.
They found that motion sickness induced by horizontal oscillation in both the
fore-and-aft and lateral direction has been shown to be dependent on the magnitudes of oscillation; the motion sickness ratings being greater as that magnitude
became greater. There was not, however, any difference in the severity of the
responses between the fore-and-aft and lateral directions.
In order to assist the prediction of motion sickness in road and rail transport,
Donohew and Griffin (2004) investigated the effect of lateral acceleration at
frequencies between 0.0315 and 0.2 Hz. They exposed groups of subjects to
sinusoidal lateral oscillation with a peak velocity of 1.0 ms−1 for up to 30 min at
one of six frequencies in that range, recording motion sickness ratings every
minute. They concluded that, for that frequency range, the probability of mild
nausea, due to lateral oscillations of the same peak velocity, increased with
increased frequency of oscillation. These results and their previous findings have
suggested that mild nausea can be predicted by an acceleration frequency
weighting independent of the frequency range 0.0315 Hz horizontal; oscillation,
in a closed cabin, for 30 min with eyes open. They found that motion sickness
induced by horizontal oscillation in both the fore-and-aft and lateral direction has
been shown to be dependent on the magnitudes of oscillation; the motion sickness
ratings being greater as that magnitude became greater. There has not, however,
been any difference in the severity of the responses between the fore-and-aft and
lateral directions, 0.25 Hz, and reduced at 12 DB per octave in the range of 0.25–
0.8 Hz. They stressed that this frequency dependence was different from that
assumed for vertical oscillation and might not apply to motion sickness provoked
by combined lateral and roll motion.
Tyler and Bard (1949) pointed out that many researchers have chosen to use
rotating devices to study motion sickness because they produced physiological
responses similar to those associated with moving vessels. They stressed that it has
been necessary to employ repeated accelerations and decelerations on such devices
in order to have the required effect on the vestibular apparatus. In addition, however, it has been desirable to add head movements while rotating in order to achieve
a more severe motion sickness response. They recounted that Spiegel et al. (1944)
designed a rotating chair which had the capability of tilting the subject’s head either
in the sagittal or frontal plane during each rotation. This caused the angle between
the horizontal plane of rotation of the chair and the horizontal or vertical semicircular canals to increase or decrease during each turn of the device. This was
found to be very effective in provoking motion sickness. Tyler and Bard were
strongly of the opinion, however, that “its effects on the labyrinth as a whole and on
the utricular maculae in particular are quite different from those produced by a
swing, an elevator, a plane or a vessel.” As we shall see later, a similar comment
had been made to me when I was designing a rotating/tilting chair for use in my
4.1 Laboratory Studies
77
cognitive-behavioural anti-motion sickness training programme (Chap. 12). It also
addresses the issue of adaptation to provocative motion and the whole question of
stimulus generalisation. This is discussed further in Chap. 7.
4.2
Motion Simulator Studies
Alexander et al. (1947) have reported upon the last of the series of studies using the
“wave machine” at Wesleyan University mentioned at the beginning of this chapter
(Alexander et al. 1945a, b, c, d). They investigated the effect of wave frequency on
the incidence of motion sickness, when the wave accelerations have been kept fixed
at 0.2 g. They used the same wave frequencies as in the previous studies, namely,
13, 16, 22 and 32 Hz with amplitudes of 9 ft, 5 ft 4 in., 2 ft 6 in. and 1 foot 1 in. In
general, they found that the incidence of motion sickness varied with wave energy.
The largest wave produced the greatest amount of motion sickness and the smallest
wave the least.
These workers then reviewed their results in relation to the four previous studies
carried out on the Wesleyan University wave machine cited earlier. In this overall
series of 5 studies, they controlled or varied the four characteristics of the waves
shown in Table 4.3. Although they concluded that their investigations of these
matters have not been complete, nevertheless, they believed that the results that are
summarized in Table 4.4 were sufficiently useful to warrant tentative conclusions
concerning the relationship between wave characteristics and the estimated incidence of motion sickness. It should be pointed out that their sickness indices in
Column 6 of Table 4.4 refer to weighted values in which vomiting is given a double
weighting (2) and lesser sickness a simple weight (1). These workers turned
their attention both to the capacity of a single wave to produce motion sickness and
the total number of waves required to do so.
In the first, third and this last study in the Wesleyan series, the time per wave
(cycling rate) has been varied, whereas it was constant in the second and fourth
studies. They observed that both a “certain intermediate wave-duration and rate of
work yielded maximum sickness.” On the basis that they believed that the rate of
motion sickness accumulated with each wave and decreased with work rate, they
concluded that wave duration was the significant variable and that an optimum
duration existed for the prescribed conditions.
In the first, second and this last study, the acceleration level was constant, but
had varied in the third and fourth in the series. The first study demonstrated wide
Table 4.3 Aspects of waves
investigated in the Wesleyan
University experiments
1. Rate of work during period of exposure (energy x frequency
of wave)
2. Energy per wave
3. Time per wave (cycling rate)
4. Acceleration-level and wave-form
78
4 Characteristics of the Provocative Motion Stimuli
Table 4.4 Summary of the effects of sixteen types of waves on the incidence of motion sickness
Code
letter of
wave
Rate of worka
(approx.) (%)
A
100
B
69
C
50
D
41
B′
69
E
52
F
31
A′
100
G
69
H
50
J
41
H′
50
K
50
L
50
M
65
N
65
J′
41
P
40
Q
38
R
35
a
With A wave as reference
Energy per
wavea (approx.)
(%)
Time per wave
(cycles per min.)
Acceleration
level (s) used
(g)
Sickness
index
100
100
100
100
100
75
50
100
100
100
100
100
100
100
100
100
100
79
55
33
32
22
16
13
22
22
20
32
22
16
13
16
16
16
21
21
13
16
22
32
0.65
0.65
0.65
0.65
0.65
0.65
0.65
0.65
0.36
0.25
0.20
0.25
0.65/0.17
0.17/0.65
0.65/0.25
0.25/0.65
0.20
0.20
0.20
0.20
10
47
63
37
33
23
10
20
77
63
53
82
15
30
38
42
53
47
10
7
variations in the incidence of motion sickness during constant acceleration and this
last study has additionally shown variations in sickness rates with a reasonably
constant work rate (wave energy wave frequency). In the third study, it had been
found that the sickness rates resulting from slow waves with low accelerations were
greater than those produced by slow waves with high accelerations, as in the first
study. On that basis, they concluded that acceleration was a significant factor. This
has been confirmed in the fourth study.
In the first, third, and fourth studies, energy per wave has been constant, whereas
it had varied in the second and current study. The incidence of motion sickness was
reduced when the energy per wave and rate of work have been reduced. In this
study, the acceleration has been constant, rate of work roughly constant and the
energy per wave and wave-duration has varied. This has shown that the energy per
wave was a significant factor in producing motion sickness. It decreased even
though the rate of energy was roughly constant. Rate of work varied in the first
three experiments, but not in the last two. In the present experiment, motion
sickness has varied despite a roughly constant rate of work. They decided that the
rate of work alone had not been a significant variable.
In general, therefore, Alexander et al. concluded that the incidence of motion
sickness depended upon wave duration, acceleration level, waveform and energy
per wave, and their inter-relationship.
4.2 Motion Simulator Studies
79
A series of studies by O’Hanlon and McCauley (1974), McCauley et al. (1976)
and Guignard and McCauley (1982) using the ONR/HFR three axis motion generator has produced a diagrammatic model for the frequency and magnitude
dependence of motion sickness for vertical z-axis sinusoidal motion in the Z axis.
These workers have shown that the most nauseogenic frequency range was from
0.17 to 0.33 Hz. These results will be discussed further in relation to the paper by
O’Hanlon and McCauley, that is reviewed next. Interestingly, apparently the
addition of pitch and/or roll to the basic vertical sinusoidal motion produced no
apparent difference in the severity of motion sickness. There has not been very
much systematic investigation of the effects of oscillatory motion in other axes.
O’Hanlon and McCauley (1974) pointed out that, for a long time, periodic
vertical motion has been accepted as the main cause of seasickness but emphasised
that, even so, the characteristics of this form of provocative motion had not been
well defined. They tested 280 subjects on the ONR/HFR motion simulator using 14
experimental conditions in randomly selected groups of 20 subjects. Each of the test
conditions consisted of a combination of particular frequency and acceleration
levels. Although the duration of exposure had been set at two hours, the test was
terminated if a subject vomited.
These workers have reported a consistent increase in the incidence of motion
sickness with acceleration, at every frequency level. Based on their data O’Hanlon
and McCauley derived a relationship between the incidence of motion sickness, in
terms of the percentage of emesis over a two hour period, and “wave frequency and
average acceleration imparted during each half-wave cycle for vertical sinusoidal
motion.” They were of the opinion that this model (see Fig. 4.1) was of practical
use, even in that elementary form. For example, it showed that “even moderate
accelerations at frequencies near 0.2 Hz should be avoided as these produce the
highest incidence of motion sickness.” The model also showed that higher accelerations at higher frequencies (e.g., 0.5–1.0 Hz) were less provocative in terms of
producing motion sickness. For these reasons, O’Hanlon and McCauley have
emphasised the importance of avoiding any “engineering strategy to ‘smooth out’ a
ride” if reducing the high-frequency motion (over 0.5 Hz) meant increasing the
energy at lower levels of acceleration, that have been associated with motion
sickness.
They noted that Kennedy et al. (1972) had already offered similar advice in the
following manner. They described what they called a “relatively benign range” of
frequencies between those that caused motion sickness (below 0.5 Hz) and those
higher frequencies that were similar to the resonance frequencies of the human
body, which lay between 4.0 and 8.0 Hz. They suggested that engineers should
make every effort to design vehicles so that most of the total energy being transmitted to the occupants lay within that frequency range known to be much less
provocative.
McCauley et al. (1976) have later performed a series of experiments on the same
motion simulator. They chose motion profiles that were beyond the vertical sinusoidal motion used in the first series, in order to further investigate potential predictors of the incidence of motion sickness. In this second series, these workers set
80
4 Characteristics of the Provocative Motion Stimuli
Fig. 4.1 Empirically derived relationship between the incidence of motion sickness: percent
emesis within two hours, wave frequency and average acceleration during each half-wave cycle,
for vertical sinusoidal motion
out to investigate the effects of additional variables on the incidence of motion
sickness. These included: the addition, to the constant vertical motion used previously, of angular motions of pitch and roll up to and beyond those expected to be
experienced at sea; habituation to the motion sickness response through daily
exposure to provocative motion; and frequencies of vertical oscillation in the range
0.5–0.7 Hz. The overall objective of this new study has been to use these new data
to refine the original O’Hanlon and McCauley model (Fig. 4.1).
The first experiment was designed to investigate the effects on the incidence of
motion sickness of adding pitch or roll accelerations to a constant vertical motion.
The most significant result in this phase of the study was that the addition of pitch
or roll has not consistently increased the incidence of motion sickness when
compared with the heave only control condition. These workers concluded that this
supported the notion that the vertical component represented the main aetiological
causative factor in producing motion sickness. At the same time, they suggested
that this observation has created doubt on the suggestion by Graybiel and Miller
(1970) and Reason and Brand (1975) that slight head movements during vertical
oscillation induced motion sickness.
The second phase of this study was designed to investigate the question of
habituation resulting from repeated exposure to vertical oscillation, by examining
differences in acceleration, duration of exposure, and the sex of the subjects. This
preliminary investigation was divided into three parts in order to investigate differences in acceleration, durations of exposure and sex differences.
In the first experiment, 20 subjects from the existing subject pool were selected
on the basis of vomiting within 2 h of exposure to sinusoidal motion at a frequency
4.2 Motion Simulator Studies
81
of 0.25 Hz and rms acceleration of 0.22 g, giving a half-wave displacement
amplitude of 4.1 ft. This has been based on the O’Hanlon and McCauley model that
predicted a 52% incidence in these circumstances. The experimenters had planned
to start the 5 daily trial exposures 5 days after the selection run, but some subjects
began after only 23 days. By definition, 100% of the subjects had vomited during
their selection exposure, however, only 75% of them did so on the first day of the
habituation trials. It was suggested that this may have been the result of a combination of three factors: (1) residual habituation, although no comments were made
regarding any difference between starting after 2 days or 5 days, (2) nonspecific
habituation or altered anxiety overlay related to the test situation (3) a regression of
subjects tested for high susceptibility toward the mean level. The results of the
5 day series demonstrated a monotonic reduction in the incidence of motion
sickness, however 6 subjects still vomited on the last two of the five 2 h exposures.
The second experiment was designed primarily to investigate the severity of the
motion profile on habituation. In addition, it included observations on the retention
of habituation and sex differences. Eight male and 6 female subjects were selected
from a total of 31 males and 8 females, using the same procedure as in the previous
experiment in this series. In this experiment, the motion profile remained the same
with the exception of the rms acceleration that had been raised to 0.33 g. According
to the O’Hanlon and McCauley model, that would have increased the incidence of
susceptibility. Again the subjects were given five daily exposures of 2 h each. In
addition, they were also given a further 2-h test one week after the final exposure in
the 5-day series in order to investigate the question of retaining habituation.
During this experiment 5 of the subjects did not complete the series, one on own
volition, 3 on unrelated medical grounds, and one due to continuing severe motion
response over the first 3 days. Regarding the remaining 9 subjects, there had been a
decrease in motion susceptibility similar to the previous experiment. This decrease
was particularly large between the first two days, with the loss of only one of the
subjects. The experimenters decided that this had not been artefactual, but the
sample size was too small to lend itself to statistical analysis. Similarly, the fact that
2 subjects appeared to retain habituation after 1 week and no significant sex differences had been observed were also considered to be tentative results.
The final experiment of this series sought to investigate the effect of the duration
of exposure on the questions of the development and retention of habituation and
issues related to the sex of the subjects. Following qualification, based on 2-h
exposures to vertical oscillation at a frequency of 0.417 Hz and 0.44 rms g
acceleration predicted to yield a motion sickness incidence of 52%, 4 male and 4
female subjects entered this study. The five habituation runs used in this experiment
were the same as in the previous, namely, 0.25 Hz and 0.33 rms acceleration.
All of the subjects completed the habituation runs but only five of the eight
subjects, two males and three females, performed the 2-h retention test. Although
the habituation results were qualitatively similar to the previous, the subject
numbers had been too small to permit significant findings. Similarly, although the
retention results seemed to indicate a lack of retention over a period of a week, the
numbers had been too small for definitive comment. Retention is an important
82
4 Characteristics of the Provocative Motion Stimuli
question, particularly for troops who are required to make ocean voyages following
different intervals of time on shore, so this question requires further study.
Overall, the results of these three experiments seemed to indicate that habituation
to provocative motion generally decreased motion responses over the 5-day period.
The greatest decrease in the incidence of sickness had occurred on the second day
and habituation had been acquired at a slower rate during the remaining three days
of the series. Comparing the results of the first two experiments in this series in
which the motion profiles had differed only in terms of acceleration, greater
habituation appeared to be acquired in the condition of greater severity of motion.
These workers likened this response to vertical motion of differing severity to the
effect on habituation of head movements during rotation. They pointed out that
Reason and Brand (1975) had cited evidence that voluntary head movements during
bodily rotation expedited the development of habituation; the main aim of the study
was to get maximum adaptation quickly and comfortably.
The results of experiments 2 and 3 were then compared. In these two situations
only the exposure times and sample sizes have differed. In the third experiment the
effects of adaptation that had been achieved by means of 1-h motion exposures each
day for 5 days were compared with the results obtained in the previous experiment
here each exposure had lasted 2 h. The motion profiles in both of these experiments
were the same, namely, 0.25 Hz and 0.33 rms g. It was found that the initial
incidence of motion sickness for the two groups has been similar, but by the third
day, the group receiving 2-h exposures demonstrated greater habituation. Similarly,
the group receiving longer exposures showed greater retention of their habituation.
Due to the small sample sizes, any possible sex difference could not be demonstrated significantly. These preliminary results have shown that five 2-h sessions of
relatively severe motion provided greater habituation and have been better retained
than either 1 h sessions with the same motion or 2 h exposures with motion of
lesser severity.
In their final study, the original database was extended to include the incidence
of motion sickness associated with vertical oscillation at frequencies between 0.5
and 0.7 Hz, using 101 male students. They used the following 4 conditions:
0.50 Hz, 0.55 rms g; 0.60 Hz, 0.55 rms g; 0.60 Hz, 0.44 rms g; 0.70 Hz, 0.55
rms g. Eight subjects were randomly exposed to a different motion condition each
day and the study continued until at least 20 subjects have experienced each condition. The results indicated that the original O’Hanlon and McCauley model, based
on data up to 0.5 Hz, reasonably predicted the incidence of motion sickness up to a
frequency of 0.7 Hz, bearing in mind the size of the sample population. They
concluded that only high accelerations, greater than 0.55 rms g, would likely
produce motion sickness at frequencies above 0.7 Hz and these might well produce
other undesirable effects, such as bodily injury, in the case of unrestrained persons.
Morton et al. (1947) noted that relatively minor changes in the types of motion
seemed to alter the incidence of motion sickness. In particular, they found that
pitching motion alone produced as much motion sickness as the combination of
pitch and roll.
4.2 Motion Simulator Studies
83
Wertheim et al. (1995b) carried out a study in their ship motion simulator at
TNO in the Netherlands to evaluate the concept, proposed by O’Hanlon and
McCauley (1974) and McCauley et al. (1976), that motion sickness was primarily
the result of heave motion and that the pitch and roll components were not significant in the aetiology of this malady. They exposed subjects in the simulator to
pitch and/or roll both with and without the addition of the heave component. They
found that roll and pitch alone seemed to provoke motion sickness and when a
relatively small heave component was added to that combination it provoked a
marked motion sickness response. As they pointed out, that relatively small amount
of heave alone did not produce a motion sickness response. They concluded that
heave, pitch and roll should not be seen as merely additive in their contributions to
motion sickness; but should be seen more in a non-linear fashion.
4.3
At-Sea Studies
Sjöberg (1968) has calculated the magnitude of ship motions to which crewmembers were exposed on board a vessel in heavy seas. He based his calculations on a
ship with a displacement of 10,000 tons, with a length of 120 m and a beam of
16 m. He has assumed a maximum pitch angle of 5° and a roll of 15°. As he has
pointed out, the oscillatory motions took place around varying diagonal axes.
However, he had chosen to simplify this feature by regarding the main oscillations
as isolated motions around the longitudinal and transverse axes through the center
of gravity.
Based on his calculations, Sjöberg made the following predictions:
1. A person located at the prow of the ship is, on pitching, thrown up and down
10–11 m, with a maximum acceleration at the turning points of approximately
2 m/s/s.
2. When at the side of the ship on a level with the center of gravity, that person is
raised and lowered 4 m, with a maximum acceleration of just under 1 m/s/s.
3. On plunging there are maximum vertical movements of 10 m, and the acceleration is about 2 m/s/s.
4. On the navigation bridge, the crewmember is thrown instead, on pitching,
forward and backward 3–4 m, with an acceleration of 1 m/s/s. On rolling he is
thrown from side to side 10 m, with a maximum acceleration of 2 m/s/s.
5. At the mast top the forward and backward movement on pitching can be 7 m
and the acceleration approximately 1.5 m/s/s, but on rolling a person can be
thrown 20–21 m from side to side, with an acceleration at the turning point of
4 m/s/s. In some cases, a person can be exposed to the sum of these vertical and
horizontal accelerations.
Pethybridge (1982) has used the information from the 1,746 respondents in his
questionnaire study of seasickness on Royal Navy ships to investigate the incidence
84
4 Characteristics of the Provocative Motion Stimuli
of seasickness on vessels on which these crewmembers have previously served. He
used these data to estimate the incidence of seasickness on individual ships and
classes of ships other than the 14 vessels involved in his current study. He found
that there was a relatively low incidence on large ships, such as aircraft and ASW/
Commando carriers, when compared to small vessels such as offshore patrol vessels
and minehunters/minesweepers. He concluded that the incidence of seasickness was
“linearly related to the square root of the ship’s weight or beam.” On that basis, he
has predicted the percentage incidence of seasickness among crewmembers
according to the displacement weight of various ships (Table 4.5). Pethybridge also
noted that those who suffered frequently from seasickness considered that the
motions of rolling, pitching, yawing, heaving, slamming and vibrating had all been
highly conducive to this malady, whereas those who suffered infrequently had listed
pitching and rolling as the most provocative movements.
Lawther and Griffin (1986) have reported on their own motion sickness questionnaire studies, which had been carried out during a number of voyages on one
particular ship. This was a car ferry that operated across the English Channel during
the daytime. The weather and sea conditions at the time had varied from relatively
calm (wind force 4, sea state 2, swell state 2) to very rough (wind force 9, sea state
7, swell state 8). During these channel crossings they recorded both the measurements of the motion of the ship and the resulting seasickness records of the passengers who took part in this questionnaire study.
These data had been obtained from a total of 4,915 passengers, involving 17
different voyages lasting up to 6 h in duration. Vertical motion had been recorded
up to 1.0 m/s/s r.m.s. and the incidence of emesis had been close to 40%. These
researchers reported that both the subjects’ magnitude estimate of motion sickness
and the incidence of vomiting were well correlated with the root mean square of the
vertical z-axis acceleration. They also noted that the duration of exposure to the
provocative motion affected the incidence and severity of seasickness. This has
suggested to them that a combined measure of acceleration (a) and time (t) should
be used to quantify the “dose” of acceleration, and found that the relation at¼ gave
the best correlation with severity of seasickness. They cautioned, however, that this
was a tentative conclusion at this early stage in their investigation.
Table 4.5 The predicted incidence of seasickness related to the displacement weight of ships
Displacement weight of ships (tons)
Predicted incidence of seasickness (%)
200
1,000
3,000
5,000
10,000
15,000
20,000
30,000
67
62
55
50
41
35
29
22
4.3 At-Sea Studies
85
Lawther and Griffin (1988) continued their survey by reviewing motion sickness
questionnaires from 20,029 passengers during 114 voyages on nine different passenger ferries around the British Isles. The duration of these various voyages ranged
from one-half to six hours, and again the sea states varied from calm to very rough.
Using the same methodology as in their previous study (Lawther and Griffin 1986),
they recorded the incidence of seasickness and other appropriate personal data from
the passengers. In addition, they obtained recordings of all six axes of motion of
each vessel. The subsequent analyses of these data allowed them to relate the
differences in the incidence of seasickness to the variations in ship motion between
each voyage and individual ships. With this information, they developed a subjective illness rating scale and used it in parallel with the recorded incidence of
vomiting.
Their raw data included ship and sea conditions that provided different motion
characteristics. Although they found a degree of correlation between the magnitudes of motion in some axes, sufficient variation remained to show that the incidence of motion sickness correlated best with the magnitude of vertical oscillation.
Lawther and Griffin then compared their data from three separate studies, and
found that there had been very good agreement in terms of motion sickness induced
by vertical oscillation. They found that the effects of the main motion variables also
produced simple mathematical approximations that could then be combined to form
general predictors. They concluded that if vertical oscillation was great enough to
cause seasickness, the additional motion in other axes could be neglected. This
supported the observation of O’Hanlon and McCauley (1974) that periodic vertical
motion was the principal factor in the aetiology of seasickness.
They noted that, over their large data set, the effect of the root mean square of the
magnitude of acceleration on the incidence of seasickness had an approximate
linear relationship. They then used this relationship to create a “normalised sickness
index” and determine the effect of the frequency of oscillation. They showed that
the greatest sensitivity to acceleration lay in the region of 0.1–0.25 Hz, and that the
steep decline at higher frequencies could be described by straight-line approximations. These, they have pointed out, could be “used to produce a frequency
weighting.”
Lawther and Griffin then addressed the question of the duration of the stimulus
using the square root of the duration to define a cumulative measure of the “dose”
of motion. They treated seasickness as a cumulative variable only since, as they
have pointed out, it was not likely that the duration of exposure would be sufficiently long for adaptation and recovery to occur. On the other hand, if longer
durations were being considered, it would be necessary to include the effects of
adaptation before making predictions of the likely incidence of seasickness.
Based on the information obtained during the British Steel Challenge 9 months
round-the-world yacht race held during 1992–1993, Turner and Griffin (1995)
reported that positive correlations had been found between sea conditions and
seasickness, both in terms of illness ratings and vomiting. This study has been
further discussed in Chap. 2 in relation to the incidence of seasickness during long
duration exposures at sea. These researchers analysed the combined data from the
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4 Characteristics of the Provocative Motion Stimuli
seven yachts in the race that reported seasickness data during the race. This was
distinct from the post-race susceptibility of crewmembers to seasickness, as discussed in Chap. 2. They found that there were no reports of seasickness at sea states
below 2. For sea conditions equal to or greater than that of sea state 6, however,
they found that 19.1% of crewmembers reported feeling ill and 14.3% of
crewmembers have reported vomiting.
These workers did not find any significant relationship between the yachts
heading and wind direction. However, they stressed that the least amount of seasickness occurred with following seas and the greatest incidence occurred when
sailing into a head wind. Wiker et al. (1979a) had previously reported that steaming
directions with head sea components caused an average of 3.5 episodes of emesis
per leg, whereas those that permitted the 95 ft Coast Guard White Patrol Boat to
steam with the primary swell caused significantly fewer episodes of vomiting (0.7
per leg).
In terms of encounter angle (0° represents ‘running’ with a following wind), the
highest percentage (19.9%) of crewmembers suffering from seasickness has been
reported for encounter angles between 120–135° and the highest percentage of
vomiting with encounter angles of 90–105°. They also found that changes in
encounter angle against the wind caused significantly greater seasickness (16.1%
reported illness and 8.0% actually vomited), when compared with no change (8.3
and 4.3%, respectively). On the other hand, they did not find any significant difference in these levels of motion sickness between changes of encounter angle with
the wind when compared to no change (6.8 and 3.1%, respectively).
4.4
In-Flight Study
It has already been pointed out in Chap. 2 that Turner et al. (2000) investigated the
relationship between low-frequency motion in short-haul turboprop aircraft and the
incidence of airsickness among passengers. They carried out a motion sickness
questionnaire survey of 923 passengers on a total of 38 UK, domestic and international flights and to the Republic of Ireland. The modified survey questionnaire
had been developed for a previous road transport study (Turner and Griffin 1999).
Two different types of aircraft were involved, namely Shorts 360 (28 flights) and
British Aerospace ATP (10 flights); durations of flights for various routes were 35
to 70 min.
In order to examine the relationship between those accelerations that passengers
experienced and the incidence of airsickness, they calculated the motion sickness
dose values (MSDV) for each of the 3 translational acceleration time histories
(lateral, vertical and fore-and-aft). These values were then correlated with the
incidence of the illness and nausea. These symptoms were found to be positively
correlated with MSDV in both the lateral and vertical direction, but not so for
fore-and-aft; and sickness has generally increased as magnitude increased.
4.4 In-Flight Study
87
Although these workers have concluded that low frequency lateral and vertical
motion might cause airsickness, they pointed out that the moderate correlation
coefficients between motion and airsickness suggested that factors other than
provocative motion could also be at play. I shall be discussing this matter further in
Chap. 6, when I suggest that cognitive factors play a very important role in the
aetiology of motion sickness.
4.5
Parabolic Flight Studies
Lackner and Graybiel (1984) evaluated susceptibility to motion sickness in the free
fall phase of parabolic flight in a Boeing KC-135 aircraft. They classed 44 male
college students with normal vestibular function as being: insusceptible, moderately
susceptible, or highly susceptible, according to their motion sickness response
while seated with head restrained during their first two parabolic flights, each
consisting of 40 parabolas. On one flight the subject was blindfolded and on the
other had a normal unrestricted view within the aircraft. Three kinds of head
movement were tested, namely, side-to-side swivel, shoulder-to-shoulder rolling,
and front-up head and trunk movements. Each subject experienced these forms of
head movement on separate days for the eyes-open and eyes-covered conditions.
The researchers found that, over all, the eyes-open condition caused earlier and
more severe motion sickness responses, irrespective of the types of head movements. Their findings also showed that front-up head and trunk movements were
more provocative than either swivel or side-to-side rolling head movements.
A further study by Lackner and Graybiel (1986b) was a continuation of their
systematic approach to determine how motion sickness susceptibility was affected
by gravito-inertial force level during the execution of natural, voluntary head
movements. This extended the work that they reported some two years before
(Lackner and Graybiel, 1984). They wished to establish whether their 1984 findings
were due to the physiological changes which had resulted from exposure to
weightlessness, per se, or if they had been caused by the high gravito-inertial force
levels of 1.8–2.0 G produced by controlled head movements during parabolic flight
manoeuvres. They found that the least provocative head movements were in yaw
with the subject’s eyes covered, whereas the most provocative were in pitch, with
eyes open. As they pointed out, these results were identical to those found during
the free fall phase of parabolic flight manoeuvres. They concluded that space
motion sickness resulted from prolonged exposure to a non-terrestrial force background rather than to free fall, as such.
DiZio and Lackner (1991) investigated a possible connection between vestibular
processing of movements of the head and space motion sickness during parabolic
flight manoeuvres in NASA’s KC-135 aircraft. In previous experiments, they found
that during parabolic flight, post-rotational nystagmus has been differentially suppressed during the period of zero G in free fall and also in a high gravito-inertial
force background of 1.8 G, relative to 1 G. They have also noted that the effect of
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4 Characteristics of the Provocative Motion Stimuli
post-rotational movements of the head on the suppression of nystagmus depended
upon the G-level. They suggested that this indicated that the velocity storage and
dumping mechanisms depended upon the level of G.
In this experiment, their aim was to measure susceptibility to motion sickness
during parabolic flight while subjects carried out head movements with their eyes
open. They rank-correlated the resulting levels of susceptibility in zero G and 1.8 G
with the following four variables: base-line conditions, namely, the time constant of
the decay of the slow phase velocity of post-rotatory nystagmus under 1 G conditions, with no head movement; the amount of reduction of that time constant in
zero G and 1.8 G conditions; the amount of reduction in the time constant produced
by head tilts at 1 G; and, finally, changes in the amount of reduction in the time
constant in zero G and 1.8 G over repeated trials.
DiZio and Lackner found that in subjects performing unregulated head movements during parabolic flight, susceptibility to motion sickness showed a significant
positive correlation with the extent to which the time constant has been reduced by
post-rotatory head movements at the 1 G level. Susceptibility was also weakly
correlated with the baseline time constant, but was not correlated with the amount
of reduction in either zero G or 1.8 G. They also observed that this suggested a link
between the mechanisms that caused space motion sickness and those of velocity
storage and dumping: “the greater the capacity for velocity storage and the more
precipitous the dumping that occurs during post-rotary head tilts in 1 G, the more
susceptible an individual is when moving about in parabolic flight.” They suggested
that if this could be confirmed by experiment, it would be a useful predictor of
susceptibility to motion sickness during parabolic flight.
4.6
Underwater Studies
Watt et al. (1996) exposed 12 subjects to repetitive pitch head movements while
they were inverted (−1 G) under water. A motion sickness rating on a 20-point
scale was recorded at the start of the experiment and then every two minutes for
20 min, or before that time if the subject reported unequivocal nausea or a score of
10, which indicated significant motion sickness that the subject had decided could
be sustained indefinitely. Motion sickness scores were then recorded every 30 min
post-test for three hours, every hour to six hours, and every six hours up to 24 h.
Subjects were also exposed to the following control conditions: 20 min stationary
in the inverted position and head pitching in the upright position. Watt et al. found
that inverted head shaking caused a significant motion sickness response in most
subjects, but not in the control conditions. In addition, they noted a marked adverse
effect on mental function, including disorientation, confusion, inability to concentrate, apathy, and drowsiness, similar to those features that have been reported in
parabolic flight. Repeated exposure to inverted provocative stimulation showed a
gradual reduction in symptomatology. They concluded that a similar type of
stimulation, lying across a bed with head tipped back during rotation, could provide
a simple means of pre-adapting to space motion sickness.
4.7 Motion Frequencies of Concern
4.7
89
Motion Frequencies of Concern
Degradations of performance occur at specific and sometimes overlapping frequencies depending on the type of stressor involved. In general, the causative
frequencies of interest lie in two distinct regions as presented in the International
Standards Organization (ISO) 2631-1 (7/15/1997), British Standard (BS) 6841
(1987), and STANAG 4154. Frequencies of motion between 0.1 and 0.5 Hz are the
most provocative of motion sickness responses. Above 0.7 Hz heave frequency,
motion sickness is unlikely unless the r.m.s. acceleration is greater than 0.55 g; it is
very important to remember the need for adequate amounts of acceleration as well
as optimal frequency to induce motion sickness. Generally the worst range of
frequencies for vertical accelerations is between 0.1–0.25 Hz, and greatest around
0.18 Hz, but must be associated with at last moderate accelerations. Above this
range, to approximately 0.5 Hz, heave motion is likely to induce motion sickness.
Whereas at frequencies above 0.5 Hz and up to 80 Hz the adverse responses are
mainly related to vibration and can affect crew health and comfort. Both motion
sickness and exposure to vibration can degrade crew performance, individually and
in combination.
These frequency ranges of interest are summarised in the American Bureau of
Shipping (ABS) Guide for Crew Habitability On Ships (12/2001), as follows:
Working and/or living on board vessels, whether conventional or high speed, can impose a
series of low-and high-frequency mechanical vibrations as well as single-impulse shock
loads on the human body.
Low-frequency vibrations (i.e., oscillations) are generally imposed by vessel motions,
which are produced by the various sea states in conjunction with vessel. Oscillation may
result in motion sickness, body instability, fatigue and increased health risk aggravated by
shock loads induced by vessel slamming. Vessel slamming may be caused by dynamic
impact loads being exerted on the vessel’s bottom or bow flare because of vessel size, speed
and wave conditions.
High-frequency vibration is often associated with high-speed rotating machinery: The
imposition of higher frequency vibrations induces corresponding motions and forces within
the human body, creating discomfort and possibly resulting in degraded performance and
health. (Griffin 1996)
No frequency is adverse in terms of performance degradation unless there is
motion of some amplitude at that frequency, In some cases, even with motion, a
particular frequency may not cause concern because of insignificant acceleration
levels. Problems with degraded performance arise when accelerations of significant
amplitudes act at particular frequencies.
90
4.8
4 Characteristics of the Provocative Motion Stimuli
Summary
• Investigators have tried to reproduce the symptoms of motion sickness by means
of artificial stimulation in an attempt to identify the causes of the symptoms of
motion sickness.
• Four basic approaches have been used, namely: swings, rotating-tilting chairs,
elevators, and complex simulators, including parabolic flight.
• Composite motion, namely: vertical, horizontal and angular, has been shown to
be more provocative than any single component. Likewise, it has been confirmed that the repetition of a combination of accelerations in different planes
creates a more potent provocative stimulus than the repetition of any of these
accelerations alone.
• If vertical oscillation is great enough to cause motion sickness, the additional
motion in other axes can be neglected.
• The most provocative frequency was shown to be 0.2 Hz, but must be associated with at least moderate accelerations.
• Studies at Wesleyan University, using a wave machine similar to an elevator,
have concluded that the incidence of motion sickness depends upon wave
duration, acceleration level, wave form, energy per wave and their
interrelationship. Total energy per wave is more provocative than the interval
between the accelerations.
• Motion sickness can be caused by purely visual stimulation, without associated
bodily accelerations.
• Studies at sea have suggested that it may be possible to predict the percentage of
incidence of seasickness based on the displacement weight of the ship in
question.
• In parabolic flight studies, subjects have been tested on side-to-side swivel,
shoulder-to-shoulder rolling and front-up head and neck movements with their
eyes open and with eyes closed. It was concluded that, overall, the subject’s
eyes-open condition caused earlier and more severe motion sickness responses,
irrespective of the types of head movements.
• Underwater studies using inverted head position showed the same symptoms as
parabolic flight manoeuvres. Repeated exposure to inverted provocative stimulation showed a gradual reduction in symptomatology.
• Frequencies of motion between 0.1 and 0.5 Hz are the most provocative of
motion sickness responses.
• At frequencies above 0.5 and up to 80 Hz, the adverse responses are mainly
related to vibration.
• Degraded performance arises when motion and accelerations of significant
amplitudes act at particular frequencies.
References
91
References
Alexander SJ, Cotzin M, Hill CJ Jr, Ricciuti EA, Wendt GR (1945a) Wesleyan University studies
of motion sickness. I. The effects of variation of time intervals between accelerations upon
sickness rates. J Psychol 19:49–62
Alexander SJ, Cotzin M, Hill CJ Jr, Ricciuti EA, Wendt GR (1945b) Wesleyan University studies
of motion sickness. II. A second approach to the problem of the effects of variations of time
intervals between accelerations upon sickness rates. J Psychol 19:63–68
Alexander SJ, Cotzin M, Hill CJ Jr, Ricciuti EA, Wendt GR (1945c) Wesleyan University studies
of motion sickness. III. The effects of various accelerations upon sickness rates. J Psychol
20:3–8
Alexander SJ, Cotzin M, Hill CJ Jr, Ricciuti EA, Wendt GR (1945d) Wesleyan University studies
of motion sickness. IV. The effects of waves containing two acceleration levels upon sickness.
J Psychol 20:9–18
Alexander SJ, Cotzin M, Klee JB, Wendt GR (1947) Studies of motion sickness: XVI. The effects
upon sickness rates of waves of various frequencies but identical acceleration. J Exp Psychol
37:440–448
Allen GR (1974) Proposed limits for exposure to whole-body vertical vibration, 0.1 to 1.0 Hz. In:
AGARD-CP-145, AGARD conference proceedings no. 145, North Atlantic Treaty
Organization Advisory Group for Aerospace Research and Development, Neuilly-sur-Seine,
France
American Bureau of Shipping (ABS) (12/2001) Guide for crew habitability on ships
British Standards Institution BS 6841 (1987) Guide to measurement and evaluation of human
exposure to whole-body mechanical vibration and repeated shock
Cheung BSK, Howard IP, Money KE (1991) Visually-induced sickness in normal and bilaterally
labyrinthine-defective subjects. Aviat Space Environ Med 62:527–531
DiZio P, Lackner JR (1991) Motion sickness susceptibility in parabolic flight and velocity storage
activity. Aviat Space Environ Med 62:300–307
Dobie TG, May JG, Fisher WD, Elder ST, Kubitz KA (1987) A comparison of two methods of
training resistance to visually-induced motion sickness. Aviat Space Environ Med 58(9,
Suppl):A34–41
Donohew BE, Griffin MJ (2004) Motion sickness: effect of the frequency of lateral acceleration.
Aviat Space Environ Med 75:649–656
Golding JF, Kerguelen M (1992) A comparison of the nauseogenic potential of low- frequency
vertical versus horizontal linear oscillation. Aviat Space Environ Med 63:491–497
Golding JF, Markey HM (1996) Effect of frequency of horizontal linear oscillation on motion
sickness and somatogravic illusion. Aviat Space Environ Med 67:121–126
Golding JF, Markey HM, Stott JRR (1995) The effects of motion direction, body axis, and posture
on motion sickness induced by low frequency linear oscillation. Aviat Space Environ Med
66:1046–1051
Golding JF, Finch MI, Stott JRR (1997) Frequency effect of 0.35–1.0 Hz horizontal translational
oscillation on motion sickness and the somatogravic illusion. Aviat Space Environ Med
68:396–402
Golding JF, Mueller AG, Gresty MA (2001) A motion sickness maximum around the 0.2 Hz
frequency range of horizontal translational oscillation. Aviat Space Environ Med 72:188–192
Graybiel A, Miller EF (1970) The otolith organs as a primary etiological factor in motion sickness:
with a note on “off-vertical” rotation. In: Fourth symposium on the role of the vestibular organs
in space exploration. NASA SP-187
Griffin MJ (1996) Handbook of human vibration. Academic Press Ltd., London (paper back
edition)
Griffin MJ, Mills KL (2002a) Effect of frequency and direction of horizontal oscillation on motion
sickness. Aviat Space Environ Med 73:537–543
92
4 Characteristics of the Provocative Motion Stimuli
Griffin MJ, Mills KL (2002b) Effect of magnitude and direction of horizontal oscillation on motion
sickness. Aviat Space Environ Med 73:640–646
Guignard JC, McCauley ME (1982) Motion sickness incidence induced by complex periodic
waveforms. Aviat Space Environ Med 53:554–563
Johnson WH, Taylor NBG (1961) Some experiments on the relative effectiveness of various types
of accelerations on motion sickness. Aerosp Med 32:205–208
Kennedy RS, Moroney WF, Bale RM, Gregoine HG, Smith HG (1972) Motion sickness
symptomatology and performance decrements occasioned by hurricane penetrations in C-121,
C-130, and P-3 navy aircraft. Aerosp Med 43:1235–1239
Lackner JR, Graybiel A (1984) Elicitation of motion sickness by head movements in the
microgravity phase of parabolic flight maneuvers. Aviat Space Environ Med 55:513–520
Lackner JR, Graybiel A (1986) Head movements in non-terrestrial force environments elicit
motion sickness. Aviat Space Environ Med 57:443–448
Lawther A, Griffin MJ (1986) The motion of a ship at sea and the consequent motion sickness
amongst passengers. Ergonomics 29(4):535–552
Lawther A, Griffin MJ (1988) A survey of the occurrence of motion sickness amongst passengers
at sea. Aviat Space Environ Med 59:399–406
McCauley ME, Royal JW, Wylie CD, O’Hanlon JF, Mackie RR. Motion sickness incidence:
exploratory studies of habituation, pitch and roll, and the refinement of a mathematical model.
Technical report No. 1733–2, Human Factors Research, Incorporated, Santa Barbara Research
Park, Goleta, CA, April 1976
Morton G, Cipriani A, McEachern D (1947) Mechanism of motion sickness. Arch Neurol
Psychiatry 57:58–70
Noble RL (1945). Observations on various types of motion causing vomiting in animals. Can J Res
23(e):212–225
O’Hanlon JF, McCauley ME (1974) Motion sickness incidence as a function of the frequency of
acceleration of vertical sinusoidal motion. Aerosp Med 45(4):366–369
Pethybridge, RJ (1982) Sea sickness incidence in Royal Navy ships. INM report 37/82, Institute of
Naval Medicine, Gosport, England
Reason JT, Brand JJ (1975) Motion sickness. Academic Press, New York, NY
Sjöberg A (1968) Experimental studies of the eliciting mechanism of motion sickness. In: NASA.
4th symposium on the role of the vestibular organs in space exploratio, pp 7–28
Spiegel EA, Oppenheimer MJ, Henny GC, Wycis HT (1944) Experimental production of motion
sickness. War Med 6:283
Stern RM, Hu S, Vasey MW, Koch KL (1989) Adaption to vection-induced symptoms of motion
sickness. Aviat Space Environ Med 60:566–572
Stern RM, Hu S, Koch KL (1993) Chinese hypersusceptibility to vection-induced motion sickness.
Aviat Space Environ Med 64:827–830
Turner M, Griffin MJ (1995) Motion sickness incidence during a round-the-world yacht race.
Aviat Space Environ Med 66:849–856
Turner M, Griffin MJ (1999) Motion sickness in public road transport: passenger behaviour and
susceptibility. Ergonomics 42:444–461
Turner M, Griffin MJ, Holland I (2000) Airsickness and aircraft motion during short-haul flights.
Aviat Space Environ Med 71:11811189
Tyler DB, Bard P (1949) Motion sickness. Physiol Rev 311–369
Watt DGD, Bouyer LJG, Pleszewski B, Kucharski W (1996) Inverted head shaking as a model of
space motion sickness. Can Aeronaut Space J 42(3):128–132
Wertheim AH, Wientjes CJE, Bles W, Bos JE (1995b) Motion sickness studies in the TNO-TM
ship motion simulator. TNO-report. TNO-TM 1995 A-57, TNO Human Factors Research
Institute
Wiker SF, Kennedy RS, McCauley ME, Pepper RL (1979) Susceptibility to seasickness: influence
of hull design and steaming direction. Aviat Space Environ Med 50:1046–1051
Chapter 5
Physiological Mechanisms Underlying
Motion Sickness
Abstract In this chapter, I shall try to provide an overview of the changes that
have taken place during the last fifty years in terms of identifying the physiological
mechanisms underlying the motion sickness response. Despite the fact that much
effort has gone into this search, we still do not have a definitive explanation for this
syndrome. I suggest that we may well find that there is no single explanation and
that perhaps a number of these current concepts are relevant. Fortunately, this lack
of a clear model for the aetiology of motion sickness has not prevented us from
making progress in terms of dealing with the condition.
Quite early on investigators began to realise that the vestibular system was implicated in the aetiology of motion sickness. For example, in 1942 McEachern et al.
had written: “it can scarcely be denied that visual, kinesthetic and psychologic
factors play a part in the development of seasickness, although the primary disturbance may lie in the vestibular apparatus or some other mechanism” (McEachern
et al. 1942). This belief gained strength and any proposal that attempted to explain
the cause of motion sickness of necessity had to introduce the role of the vestibular
system in that mechanism. Unlike McEachern et al., many of these researchers have
concentrated almost wholly on the role of the vestibular apparatus and have tended
to ignore the fact that other special senses have contributed to the body’s
orientation.
As Gay (1954) has observed:
Studies of the labyrinth have crystallised the conclusion of most observers that the labyrinth
is the most important anatomical area in the causation of motion sickness. The primary
function of the semicircular canals is to register changes in the rate of motion acceleration
or deceleration and in the direction of motion. Various techniques to stimulate the labyrinthine structures have yielded much information; for example, rotation of the body, caloric
stimulation through syringing the ear with hot or cold water, and galvanic stimulation.
Despite the fact that much has been written about the physiological correlates of
motion sickness, together with associated aetiological models, the underlying
neurophysiological processes are by no means clear. Nor do we yet know which
particular centres and pathways within the central nervous system are involved in
© Springer Nature Switzerland AG 2019
T. G. Dobie, Motion Sickness, Springer Series on Naval Architecture,
Marine Engineering, Shipbuilding and Shipping 6,
https://doi.org/10.1007/978-3-319-97493-4_5
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5 Physiological Mechanisms Underlying Motion Sickness
either the cause of the various motion sickness responses or the process of adaptation to provocative motion.
We know that certain researchers considered that the vestibular apparatus and its
projections in the cerebellum were necessary to the development of motion sickness. For example, in canine experiments, Wang and Chinn (1956) and Bard et al.
(1947) have demonstrated that the cerebellar nodulus and uvula were essential to
the susceptibility to swing sickness. Wang and Borison (1950) and Wang and
Chinn (1954) have identified a “vomiting centre” in the brain stem that received
inputs from various sources, both central and peripheral, such as the diencephalon
and the gut. Both Wang and Chinn (1954) and Brizzee and Neal (1954) have
reported that an intact vomiting centre in the area of the fasciculus solitarius,
together with a closely related chemoreceptive trigger zone (CTZ) in the area
postrema on the floor of the fourth ventricle were necessary for provocative motion
to produce vomiting. More recently, however, Oman (1990) has reported that
attempts to reproduce these experimental results have been unsuccessful and have
led workers to “doubt that medullary emetic centers are discretely localizable.”
Further work is required before we have a clearer picture of the physiological
underpinnings of this distressing condition.
5.1
Vestibular Overstimulation Theory
Although the mechanism has not yet been determined with absolute certainty,
changing acceleration acting on the labyrinth in the inner ear is clearly a basic cause
of motion sickness (McNally and Stuart 1942). This is indicated by two observations: first that the incidence and severity of motion sickness are closely related to
the duration and severity of such accelerations; and second, individuals without
functioning labyrinths are immune to this condition.
Since experimenters have first realised that the vestibular system was the location of the specialised sense organs which transduced angular and linear motion
stimuli, and that the absence of the vestibular end-organs results in complete
immunity to motion sickness (James 1882; Reynolds 1884; Minor 1896; Sjöberg
1929; Kellogg et al. 1964; Kennedy et al. 1968), many have believed that this
malady was the result of vestibular overstimulation. This cannot be. Many large and
unfamiliar stimuli, such as sudden stops in a rotating chair, are not provocative,
whereas much smaller physical stimuli, such as cross-coupled (Coriolis) accelerations in a rotating/tilting chair, can be highly provocative. In addition, motion
sickness can be produced by visual stimulation alone, with no vestibular activity
involved.
Graybiel (1970) has investigated 12 subjects with visual defects under conditions of stressful Coriolis accelerations. These subjects have exhibited differences in
their susceptibility to motion sickness that showed no relationship to the rank order
of their visual deficits. As far as they have been able to demonstrate, visually
impaired individuals have shown no significant differences in susceptibility to
5.1 Vestibular Overstimulation Theory
95
motion sickness when compared with normal control subjects. Graybiel concluded
that vision was not an essential factor in the aetiology of motion sickness rather that
it was a secondary feature. He has stressed, however, his conviction that this
observation did not contradict the fact that symptoms characteristic of motion
sickness may be induced by visual stimulation in the absence of a motion input.
Oman (1990) has pointed out other serious limitations in the vestibular overstimulation theory. Individuals adapt to specific motion environments with experience. Assuming similar experience individuals in active control, such as piloting
an aircraft or driving a car, are less prone to motion sickness than are the passengers. Oman has also suggested that self-generated sensory stimulation such as
that involved in sporting activities rarely cause motion sickness unlike externally
generated motion stimulation. He has concluded that these factors strongly contraindicated overstimulation of the vestibular apparatus as a reasonable explanation
for the aetiology of motion sickness.
5.2
Sensory Conflict Theory
The concept that motion sickness is caused by vestibular overstimulation has been
replaced by the sensory conflict theory. This hypothesis has proposed that the
physiological component was not simply a single vestibular event, but rather that it
was the body’s response to inharmonious sensory information reaching the
so-called comparator in the brain. Provocative motion stimuli, whether they originated from active or passive bodily motion, are mainly detected by the eyes and the
vestibular apparatus. However, changes in the body’s orientation to the gravitational field and other added linear accelerations can also stimulate mechanoreceptors located in the skin, muscles, joints, and other bodily tissues.
Passive provocative stimuli are caused by the body being moved by some form
of vehicular motion. In addition, an active component may be caused by bodily
movement, such as moving the head, which also affects the vestibular apparatus.
The restriction of head movement has already been mentioned in Chap. 2 as a
means of preventing airsickness (Johnson et al. 1951; Johnson and Mayne 1953).
One of the earliest proponents of the sensory conflict theory as an explanation
for the cause of motion sickness, was Irwin (1881), who has described his views as
follows: “In the visual vertigo of seasickness there appears to be a discord between
the immediate or true virtual impressions and a certain visual habit or visual sense
of the fitness and order of things, which passes into consciousness as a distressing
feeling of uncertainty, dizziness and nausea.” Some time later, Claremont (1931)
published a full description of the sensory conflict theory. Since then, there have
been a number of papers on that subject, including those by Hill (1936), Morales
(1946), Lansberg (1960), Steele (1970), Guedry (1970) and Reason (1970).
Norfleet et al. (1995) have utilised inverted immersion as a means of rotating the
gravity vector through 180°, so that it was opposite to its normal direction. This
produced sensory conflict between the otolithic input and the afferent signals from
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5 Physiological Mechanisms Underlying Motion Sickness
the eyes, proprioceptor sources and the semicircular canals. They have postulated
that this conflict should cause more severe motion sickness than upright immersion
in which the vestibular end organs were still affected by gravity, as if the subject
had not been immersed. They briefed the 9 male certified SCUBA divers who took
part in their experiment to stop the test with the onset of persistent nausea.
They found that none of the subjects has experienced the onset of persistent
nausea and, therefore, all were able to complete the three-hour test during upright
immersion. During inverted immersion, however, 7 of the subjects terminated the
test and only the remaining 2 completed the three-hour exposure. In addition to the
increased severity of motion sickness during inverted immersion, the subjects had
also demonstrated a greater impairment of postural stability compared with upright
immersion. Norfleet et al. have concluded that inverted immersion permitted an
easy, inexpensive means of studying sensory conflicts arising from inharmonious
otolithic inputs.
Coats and Norfleet (1998) continued immersion studies in the Weightless
Environment Training Facility pool at the Johnson Space Center. In this series,
however, they used a new experimental model that consisted of an enclosure that
was immersed in the pool, either upside-down or in the front-down position. The
walls of the enclosure were lined with large posters that provided visual cues that
denoted an upright position. The visual vertical was also indicated by 8 clock faces
mounted on the front and rear walls near the corners of the room, plus a chair
attached to the floor and lights mounted on the ceiling of the room. In the study,
there were 19 male and 3 female subjects who alternately set each of the 8 clocks
and made exaggerated bowing head movements.
The researchers found that in the room-inverted position, the incidence of
motion sickness has been 56% compared to 36% when the room was in front-down
position. Although the pitching head movements have been found to be the most
provocative actions, the clock setting tasks were almost as provocative, particularly
when the clock filled the subject’s visual field.
In this study, the end-point of a test was defined as the onset of stomach
awareness compared with persistent nausea as used by Norfleet et al. in the previous
study, thereby preventing direct comparison of the results. Unlike the previous
study, Coats and Norfleet found no decrement in postural stability however, as just
stated, their motion sickness end-point had been less severe. They also reported that
susceptibility to terrestrial motion sickness, measured by a subjective questionnaire,
correlated highly with the susceptibility in the false vertical room. Finally, they
found that the inverted and front-down positions of the room caused motion
sickness, unlike the upright position that did not. They concluded that the false
vertical room might provide a useful terrestrial model of space motion sickness
despite the fact that there were several differences in the sensory environment.
5.3 Neural Mismatch Hypothesis
5.3
97
Neural Mismatch Hypothesis
In 1978, Reason proposed a change to his understanding of the sensory conflict
theory which, up to that time, had been based on the assumption that conflict had
resulted from a direct comparison of afferent signals arriving from different sensory
modalities. Reason has suggested that the concept that a direct comparison in which
inputs from the eyes and ears, for example, took place somewhere in the central
nervous system was not acceptable. He then introduced his neural mismatch
hypothesis based on the “reafference principle” of von Holst (1954) and the
“sensory rearrangement” theory of Held (1961). Reason’s concept implied that the
situations that provoked motion sickness were characterised by a “condition of
(sensory) rearrangement.”
The expression “sensory rearrangement” had first been used by Held to describe
experimental situations in which information arriving at certain receptors was
sufficiently distorted that it was no longer compatible with inputs to other receptors
with similar functions. In the early stages of rearrangement, before a person has
become adapted to the new situation, there was a state of conflict between the total
arrangement of sensory input and that which has been expected on the basis of that
individual’s past experience. This was what Held has called “exposure-history.”
Subsequent adaptation to this sensory rearrangement has been considered to require
the neural state to be updated with new sensory and motor “memory trace” pairs.
In the context of motion sickness, not only did the concept of sensory rearrangement indicate that the incoming signals from the various bodily receptors were
at variance with each other, they were also in disagreement with those that the brain
had expected to receive. The comparison of the sensory inputs with an engram
based on previous experience was critically important to the concept. This implied a
neural center within the central nervous system that fulfilled the function of a
comparator of both the afferent signals from the various sensory end organs and the
neural store of signals from the internal model. In turn, if any sustained difference,
or mismatch, between this actual information and that which had been expected had
enough intensity, it both modified the internal model and caused the neurovegetative responses that we recognised as motion sickness.
Reason summed up the sensory rearrangement theory as having two main features: first, that the motion sickness responses were due to a “conflict between the
present sensory information and that retained from the past” (Reason 1978), and
second, that irrespective of what other spatial senses were party to the these conflicts, the vestibular system must be implicated, either directly or indirectly (as in
visually-induced sickness) for motion sickness reactions to ensue.
Reason opined that there could be many forms of sensory rearrangements
depending both upon the circumstances at hand and as a consequence of the
associated sensory input modalities involved. Although he referred to six kinds of
sensory rearrangement that could cause motion sickness, he suggested that two
main types were commonly described according to the receptors involved:
visual-inertial rearrangements in which “inertial” included both the vestibular and
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the non-vestibular proprioceptors and the (semicircular) canal-otolith rearrangements. In each case, two types of conflict could occur. In the first situation, known
as Type 1, both systems signalled contradicting or uncorrelated information at the
same time. In the second situation, known as Type 2, when one system was sending
information, there was an absence of the expected signal from the other.
Numerous examples of these mismatches have been given by various researchers
in terms of both everyday and laboratory experiences (Reason 1975).
5.4
Visual/Inertial Rearrangements
In Type 1 visual/inertial mismatch, the motion inputs from the eyes and vestibular
or non-vestibular proprioceptors are contradictory, such as may occur when reading
a hand-held book in an automobile, or a map in an aircraft when flying in rough air.
A classic example of this form of motion sickness can be demonstrated with optical
devices that either invert the wearer’s visual field or reverse it laterally. In this
situation, either active or passive movement of the head, as indicated by the
vestibular apparatus, alters the visual picture in an unexpected way. At sea, if one
looks over the side of the boat at the waves while the vessel is pitching, the ship’s
movement will not appear to be correlated with the apparently random movement
of the waves. This produces a conflicting visual stimulus likely to provoke seasickness. On the other hand, if one looks at the horizon, there is a steady reference
against which to sense whole body motion correctly. Another example of this type
of mismatch is the pseudo-Coriolis effect (Dichgans and Brandt 1973) induced in an
optokinetic drum when a subject tilts his or her head in the coronal plane during, or
shortly after, experiencing circular vection. Circular vection is discussed in
Chap. 13, when we are discussing Cognitive-Behavioural Training.
There are two kinds of Type 2 visual/inertial rearrangements, namely, those
caused by visual cues without the usually expected inertial input, or vice versa,
inertial cues without the expected visual input. The first of these, Type 2a, can be
produced by dynamic visual displays, where the observer is not exposed to actual
motion, such as in a fixed-base simulator. Type 2b conflict is experienced in all
forms of passive transport if the subject does not have a clear view of the outside
world. For example, this occurs below deck in a ship where there can be vestibular
and kinesthetic stimulation in the absence of visual motion cues, since the cabin
walls, floor, and the person standing on the floor are all moving together and there
may be no relative movement detected by the eyes.
5.5 Canal/Otolith Rearrangements
5.5
99
Canal/Otolith Rearrangements
Type 1 canal/otolith rearrangements occur when one’s head is moved in a rotating
environment. This occurs during cross-coupled (Coriolis) stimulation (a subject
which is discussed later, in Chap. 11). It should also be remembered that the signal
from the canals that have been stimulated persists for some 10 s after the movement
has ceased due to the recovery time of the endolymph within the canals. The
microgravity of space shuttle missions is an example of Type 2 rearrangements,
where the semicircular canals are stimulated without a corresponding input from the
otoliths (and other gravireceptors). In the case of heave motion on board ships, the
otoliths are exposed to linear acceleration, which is changing in magnitude and
direction in the absence of a corresponding signal from the semicircular canals. This
rearrangement is even greater at low frequency (<0.5 Hz) because, during linear
motion, the otolithic response can be out of phase with the inputs from both the
muscle and joint mechanoreceptors, and also from the eyes.
Guedry (1991) has made the point that the description sensory conflict does not
fit certain stimulus conditions that cause motion sickness. As an example of this, he
has cited that many astronauts suffer from space motion sickness during the first
few days of a mission, until they become adapted. He has suggested that in this
situation, “we have sensory messages not clearly in conflict with one another, but
rather sensory messages in combinations that can’t be immediately interpreted by
the brain networks that generate sequences of motor reflexes that ordinarily improve
the quality of motion control.” For that reason, Guedry prefers the term “neural
mismatch” to characterize the stimuli that cause motion sickness.
The idea that a model of the afferent and efferent activity, identified with bodily
movement, is present in the central nervous system comes from two sources, work
carried out on sensory motor processing (von Holst 1954), and other studies on
adaptation (Held and Mikaelian 1964).
5.6
Vestibular/Proprioceptor Mismatch
Guedry (1991) has also proposed this third category of neural mismatch, which he
has deduced from the significantly different reactions that result from active and
passive motion. He has pointed out a marked difference in perceptual responses,
oculomotor reflexes and trunk and limb reflexes when one has compared these
during and after prolonged active turning with these responses when they have
occurred before and after passive turning. As Bles (1996) has pointed out, this
particular mismatch combination is becoming more significant as virtual reality
plays a greater role in the variety of today’s wider range of training systems.
Quite naturally, the human body is designed for the acts of walking, running, or
jumping on the surface of the Earth. Consequently, during the performance of these
natural manoeuvres, the main acceleration frequencies reaching the head lie
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somewhere between 0.5 and 8 Hz, so linear oscillation at 1 Hz does not produce
motion sickness. On the other hand, oscillation at 0.2 Hz is highly provocative and
this is probably due to the nature of the engram, based on canal/otolithic activity that
has been established during these locomotor activities on the Earth (Benson 1984).
The comparator in the brain has built up a model of the various inputs and outputs
associated with body position and bodily movement. This engram is based on
experiences of everyday locomotion on Earth. A commonplace example of this is the
act of stumbling that frequently occurs when a person steps onto a stationary escalator. The engram associated with approaching an escalator is based on the corrective
movements necessary to step onto a stairway which is usually in motion; hence the
tendency to stumble when it is not. A similar situation occurs when a subject stops a
treadmill. This response is not related to the peripheral visual stimulus that causes
vection; it is based upon expected signals from previous experiences of an environment that is normally moving. Brief mismatches cause immediate corrective
muscular responses. Sustained mismatch signals, on the other hand, reprogramme the
internal model in the comparator, by adaptation. This adaptive process does not occur
immediately, however. The time delay during which this takes place also varies
greatly with both the individual and the particular provocative environment. In
general, the most rapid gains occur quite early, after which the rate of adaptation
becomes progressively slower. In the meantime, the rearrangement that has been
created triggers the bodily responses that we know as motion sickness. Benson’s
(1988) diagrammatic representation of the functional components and processes
contained within this physiological model of motion sickness are shown in Fig. 5.1;
this will be discussed again in the next chapter, when introducing Dobie and May’s
psychophysiological model based on this model by Benson.
Fig. 5.1 A diagrammatic representation of Benson’s physiological model of motion sickness
5.7 Heuristic Mathematical Model
5.7
101
Heuristic Mathematical Model
Oman (1990) has described Reason’s (1978) model as having several important
deficiencies. It has failed to explain why certain forms of stimulation cause motion
sickness and gave passive vertical low frequency linear acceleration as an example.
For example, he has stressed that since Reason’s model was qualitative, it was,
therefore, incapable of either simulation or of making measurable estimates of
response. He also noted that there was an absence of information on the question of
the purpose of the sensory conflict signal to the person since it only seemed to be
related to the end result of motion sickness. He further pointed out also that there
was a lack of any information on neural pathways that must be present in order to
account for the particular time course of motion sickness symptomatology.
Given what Oman has seen as the deficiencies of Reason’s model, he believed
that it called for a reexamination of the theory; an attempt to quantify it and finally
to relate it to other models describing the perception of spatial orientation. In so
doing, he has provided a preliminary heuristic model that associated the incidence
and severity of motion sickness and was related to the magnitude of the difference
between a vector representing all sensory input and another representing the
expectancy of that information. Although not validated experimentally, Oman
believed that the model carried significant conceptual validity for a number of
reasons. It has included and expanded upon many of the earlier qualitative models
and in so doing, seemed to overcome some of their shortcomings. It has taken into
consideration experimental evidence for the control of preprogrammed movement.
It has also included information related to the production of motion sickness
symptoms similar to the time course of symptoms shown experimentally. Although
Oman has stated that the system’s approach to explaining motion sickness is
attractive, he has recognised that many of the underlying physiological mechanisms
are only represented in abstract and assumptions have been made beyond our
current knowledge of neuronal mechanisms.
5.8
Subjective Vertical Conflict Theory
Bles, for his part, has proposed an extension of a concept proposed by Oman in that
“motion sickness may be provoked only in conditions where there is a mismatch
between the computed subjective vertical based on the incoming sensory information and the one computed by the internal model.”
Bles et al. (1998) have observed that it was difficult to place a particular example
of provocative motion into one of the many specific conflict categories described by
Reason and Brand (1975) and Reason (1978). They have further pointed out that,
although accepting that most of the different conflicts described by Guedry (1991)
might cause disorientation, motion sickness was the result of disparity between the
subjective vertical, based on previous experience, and the sensed vertical
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determined by sensory input. These workers put forward a theory of the aetiology
of motion sickness based on the individual’s subjective determination of the
internal representation of the vertical. They postulated that there was only one
significant conflict and that is the difference between the expected and the sensory
vertical and they have suggested that verticality is critically important to the
maintenance of an upright posture. They have also noted that this feature has been
supported by Riccio and Stoffregen (1991) who have proposed that the control of
bodily orientation provided a better understanding of the aetiology of motion
sickness than did the sensory conflict theory.
5.9
Postural Instability Theory
Stoffregen and Riccio (1991) are of the opinion that most of the work related to the
study of motion sickness has been based on the same basic suppositions and which
lead to representations of perception and action that are incorrect. As a result, they
have concluded that the sensory conflict theory did not provide a satisfactory and
tenable explanation for the motion sickness response.
Riccio and Stoffregen (1991), having renounced the sensory conflict theory on
the basis that it might not exist, have put forward a fundamentally new proposition
for understanding the aetiology of motion sickness based on an ecological concept
of the underlying control of orientation. They postulated that animals experienced
sickness when they were incapable, for whatever reason, of maintaining a stable
posture. They have suggested that this instability, which occurred prior to the onset
of the symptoms of motion sickness, was a necessary prerequisite of this response.
5.10
Other Intermodality Conflicts
Mittlestaet has observed (referred to by von Gierke and Parker in 1994), that human
gravireceptors located in the trunk might transduce acceleration through the
movement of the abdominal viscera. They examined this finding in terms of the
perception of bodily position and the motion sickness response. They were of the
opinion that a possible sensory conflict could occur between the inputs from the
vestibular and visceral graviceptors. These workers then pointed out that the frequency range of this potential conflict was relevant to practical applications in terms
of responses to provocative motion. It corresponded to the principal frequency
range for inducing motion sickness in certain forms of transport, namely around
0.3 Hz. They also opined that it could account for the motion sickness occurring
during rotation around Earth-horizontal axes. As they pointed out, the incidence of
this malady was high during barbecue-spit stimulation (subject’s z-axis) and during
x-axis rotation, whereas it was less severe during y-axis stimulation. They also
suggested that these differences between the otolithic and visceral gravireceptor
5.10
Other Intermodality Conflicts
103
inputs could account for the inversion illusion found during parabolic flight profiles
performed in space motion sickness research. It could also have caused incorrect
perception of vertical oscillations that were common to helicopters operations. They
concluded that further studies were warranted to better understand these systems
and their interaction.
Referring to the observation that head and body movements made in microgravity tended to cause motion sickness, Lackner and DiZio (1991) remarked that
they have been associated with unusual combinations of semicircular canal and
otolith activity, compared to similar head movements made on Earth. They
attributed this situation to the unloading of the otoliths in zero gravity. They also
pointed out that subjects performing head movements while exposed to visual
inversion (or reversal) on Earth also experienced motion sickness, “because the
vestibulo-ocular reflex is rendered anti-compensatory.” In their 1991 study, these
researchers showed that susceptibility to motion sickness during exposure to visual
inversion was decreased in a 0 G environment, compared to 1 G. They suggested
that this seemed to be related to a change in the function of the otoliths in a zero-G
environment. Lackner and DiZio have concluded that their findings indicated that
“motion sickness is evoked when oculomotor and retinal slip signals are consistently inappropriate for the orientational information provided by vestibular activity,” and that head movements were more provocative when there was a mismatch
between the output from the otoliths and semicircular canals and the retinal and
oculomotor signals. Finally, they concluded that like motion sickness on Earth,
space motion sickness could be caused by many different factors, including many of
the afferent and efferent pathways involved in the control of movement and
orientation.
Pointing out that it is commonly held that space motion sickness was caused by a
“conflict” between vestibular, visual, and other sensory inputs, Leigh and Daroff
(1985) have reviewed three specific hypotheses for the aetiology of space motion
sickness. First, von Baumgarten and Thumler’s (1979) proposal that a slight difference in the weight of the otoliths which, in Earth’s gravity, was adequately
compensated by neural mechanisms created vestibular imbalance during exposure
to zero gravity. Second, Lackner and Graybiel’s (1981) opinion that zero gravity
caused a decrease in the gain of the horizontal vestibulo-ocular reflex so head
movements created a visual-vestibular conflict. Third, Matsuo and Cohen’s (1984)
proposal that upward-downward asymmetries of the vertical optokinetic responses,
being otolith-dependent, would be greatest in a zero gravity environment which
could lead to a visual-vestibular conflict during vertical head movements. Leigh and
Daroff pointed out that in each of these three hypotheses, abnormalities of eye
movement would be expected, and they have identified the characteristic disorders
of ocular motility associated with each of these three hypotheses. They have
emphasised, however, the marked technical difficulties involved in recording horizontal and vertical eye movements accurately during free head movements in space
flight. They have further suggested that careful clinical examination aimed at
identifying those specific abnormalities that were predicted by each of these three
hypotheses might be a practical alternative worthy of consideration.
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In order to clarify the resultant difference between the effects of wearing horizontally and vertically reversing prisms on spatial orientations, Takahashi et al.
(1991) studied locomotion and motion sickness, using 10 normal subjects and a
patient with bilateral labyrinthine loss, during exposure to reversed vision. They
found that when vision has been reversed horizontally, both motion sickness and a
moderate to severe disturbance of gait has occurred in all normal subjects, whereas
vertical reversal of vision failed to produce either. The patient who did not suffer
from motion sickness during either type of reversal, due to labyrinthine deficiency
was, however, unable to walk straight during horizontal reversal.
These researchers also noticed that horizontal head movements have been
greater than vertical when the subject was walking, whereas vertical head movements were greater when running. While subjects walked in an open space, the
number of voluntary head movements was observed to be greater in the horizontal
plane, in order to observe the surroundings or change direction. They have noted,
however, that neither running nor repeated pitch movements caused motion sickness during vertical reversal of vision and concluded that the magnitude of the
provocative stimulus was probably not a significant cause of motion sickness.
These workers believed that the difference in the magnitude of the sensory mismatch between the reversal directions seemed to be due to the different role of
vision in providing spatial orientation, which has been produced by both proprioceptive as well as otolithic inputs of gravity.
5.11
Treisman’s Evolutionary Hypothesis
Treisman (1977) has suggested 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.” The purpose of his
paper has been to identify the aetiology of motion sickness and to propose an
evolutionary interpretation. He has first proposed that motion sickness was initiated
by “repeated challenges to redetermine the relations of the eye-head or the
head-body systems, or both,” and not by movement itself. He suggested that
provocative situations could be due to a lack of familiarity with the particular
challenge or because it was greater than a person’s level of adaptation. Although
this suggestion is similar to the sensory conflict theory (Reason and Brand 1975),
Treisman believes that the conflict differs. He has suggested that the provocation
was not so much between the current sensory input and a subject’s past experience,
instead he postulated that two closely coupled spatial reference systems needed to
be monitored continuously and simultaneously if they were to be able to perform a
motor task. In the meantime, other irregular or unpredictable disturbances upset the
existing harmony between the systems.
He further stated that the systems that control movement, including eye movement, and determined the body’s position in space, were almost always complex
5.11
Treisman’s Evolutionary Hypothesis
105
and highly susceptible to minor disturbances. For that reason, he suggested that
they could provide an “ideal warning system for detecting early central effects of
neurotoxins.” He suggested that naturally occurring toxins affecting the nervous
system were likely to alter sensory input, motor coordination, or both. He has
pointed out that an emetic response to such mismatches would, for example, be “an
advantageous adaptation for an unspecialized feeder which might ingest neurotoxins in vegetation or carrion.”
Treisman concluded that it was unfortunate that many of today’s novel situations, such as vehicular travel, should provide a similar provocative stimulus in
man. If it were true, however, both motion sickness and food poisoning would
fulfill the same biological function. Treisman described motion sickness in such
cases as “an adaptive response evoked by an inappropriate stimulus.” As he has
pointed out, the act of vomiting is an appropriate means of eliminating toxins, and
the associated malaise and nausea might contribute to aversive conditioning. I have
already stated my belief that motion sickness is a protective response occurring in a
normal individual reacting to an abnormal situation. I also concur with his view that
provocative situations could be due to a lack of familiarity with a particular challenge, or because it was greater than a person’s level of adaptation. However, I
strongly believe that an individual’s past experiences are also particularly important, as we shall see later, because that past experience could either sensitise the
individual to provocative motion or aid in adaptation, depending on the duration
and nature of the motion. This will depend a lot on a child’s introduction to
provocative motion; for example, were these early exposures long or short, frequent
or infrequent in rough or smooth conditions.
Money and Cheung (1983) have surgically removed the vestibular apparatus of
the inner ear in seven dogs and found that the emetic response to lobeline, levodopa, and nicotine has been impaired. They concluded that it was reasonable,
therefore, to suggest that the inner ear was part of the normal physiological
mechanism for producing a vomiting response to poisons, and that it was likely,
therefore, that this mechanism produced a similar response to provocative motion.
However, the surgery had no consistent effect on the dog’s emetic response to
pilocarpine or apomorphine. These negative results with apomorphine confirmed an
earlier finding reported by Wang and Chinn (1956). Although it seemed unlikely,
therefore, that the vestibular apparatus played a significant role in the dogs’ emetic
response to apomorphine, Money and Cheung noted that in man recumbency
offered some protection against vomiting induced by apomorphine. In addition,
they pointed out that in seated, as distinct from recumbent conditions, in subjects
the severity of the apomorphine response differed according to the orientation of the
head to the direction of gravity (Isaacs 1957). These workers have suggested that
this perhaps indicated the existence of differences between species, pointing out that
it has already been reported that different species showed different responses to
provocative motion (Money 1970) and different responses to both emetic and
antiemetic drugs (Brand and Perry 1966; Laffan and Borison 1957).
Money and Cheung (1983) have questioned why the response of the vestibular
apparatus varied in the way in which it seemed to facilitate vomiting with different
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5 Physiological Mechanisms Underlying Motion Sickness
poisons. As they pointed out, there were many ways by which poisons could cause
vomiting and postulated that the vestibular apparatus might only be involved in
some of these mechanisms. They have also queried how these mechanisms operated. They have suggested that, under normal circumstances, the vestibular apparatus might have a tonic effect on some of the central emetic systems. In which case,
if that action were removed, or if certain of these central mechanisms related to the
motion sickness response degenerated following labyrinthectomy, one could expect
the emetic reaction to be impaired. They have also supported Treisman’s suggestion
that the presence of poisons in the cerebral circulation could reduce conflicting
inputs from vestibular, visual, and other proprioceptive sources. Perhaps, then, the
brain interpreted these conflicting inputs as indicators of poisoning and the
necessity to recalibrate the systems. If so, the removal of vestibular inputs by
labyrinthectomy would explain the resulting impairment of the emetic response.
Money and Cheung have observed that the evidence from their current experiment
was consistent with both of these suggestions.
Money and Cheung have championed Triesmsan’s evolutionary hypothesis on
the grounds that it provided a reasonable explanation for the developmental
involvement of the inner ear in the act of vomiting. In addition, this explanation was
also consistent with the mismatch theory of motion sickness and coherent with all
the scientific evidence concerning the characteristics of the stimuli that provoked
motion sickness. They concluded that the aetiology of motion sickness now seemed
“to make sense.” In a provocative motion environment, the brain, in effect, says:
“This unusual requirement for recalibration is such that my vestibular system must
be sending me false information; therefore I have probably been poisoned by
something I ate, and I should vomit.”
5.12
Nystagmus Hypothesis
Ebenholtz et al. (1994), on the other hand, have proposed a different explanation for
the occurrence of motion sickness. Rather than the classical conflict theory, their
suggestion has been based upon the oculocardiac reflex, namely, the bradycardia
produced by extra-ocular muscle traction (Milot et al. 1983) and the reported
occurrences of emesis following surgical correction of strabismus (Houchin et al.
1992). It has been proposed that this traction of the eye muscles produced afferent
signals running from the ciliary ganglion to the trigeminal and vagus nerves (Katz
and Bigger 1970). The same pathway was presumed to have been activated during
reflexive eye movements under the control of the vestibular apparatus and during
eye movements that have been activated by a mixture of both reflexive and voluntary stimulation. For these reasons, they have made the logical proposal that, in a
provocative motion environment, motion sickness would be prevented if the
afferent signals from the extra-ocular muscles were blocked, assuming an otherwise
intact vestibulo-ocular system.
5.12
Nystagmus Hypothesis
107
These workers stated that they believed that, since there was a close association
of eye movements and the vestibular system and, in addition, the vestibular system
also played a central role in the sensory conflict or neural mismatch theory, it was
most likely that eye movements played a significant part in all of these sensory
conflicts. They have suggested, therefore, that every nauseogenic situation included
in these various sensory conflicts could involve a difference of eye movements,
which were being controlled by separate oculomotor systems. As an example, they
quoted the effect of cross-coupled (Coriolis) stimulation wherein the eyes experienced both otolith-driven ocular torsion and a complex pattern of nystagmus due to
stimulation of both horizontal and vertical semicircular canals. They proposed that
this combination of torsion and nystagmus could cause a traction-induced afferent
input, producing vagal stimulation. They have also pointed out that there were
many other visual-vestibular conflicts that could include active and competing
oculomotor systems at the same time.
They have cited a flight simulator capable of portraying low-level, high-speed
flight to exemplify this situation. In such a situation, the trainee was presented with
a high-speed optokinetic pattern that required matching eye and image velocity. In
addition, a moving target with a velocity profile different from its background
would cause the trainee to follow by means of foveal pursuit. These eye movements
would likely take place during subjective head movements and simulator motion.
These interacting complexities would include a vestibulo-ocular response that
might describe a trajectory quite different from either that of the optokinetic
response or the foveal pursuit. As they pointed out, “the latter is designed as a
negative feedback system,” so that error correction driven by slip signals would
occur and fixation or tracking would only succeed within a certain range of target
frequencies. They have emphasised that, in such a scenario, so many reflexive
oculomotor systems were active that there was likely to be significant eye muscle
traction with ensuing afferent output.
Finally they have pointed out the possible significance of a previous observation
that asthenopia, which Ebenholtz (1988) has described as “a visually-induced
variation of motion sickness,” was considered to be caused by many small, corrective eye movements which created an effect with the passage of time. However,
Ebenholtz et al. have also suggested that it was possible for a single exposure to a
rapid, high velocity eye movement to induce motion sickness. As we have already
reported, simulator sickness is very prevalent and wastes a considerable amount of
training time. This is a very interesting hypothesis that merits further study.
All of these factors must be taken into account when explaining the underlying
cause or causes of motion sickness. Indeed, the results of a study in our laboratory
on the UNO campus have suggested an interactive model of motion sickness in
which both sensory conflict and eye movements play their part in explaining the
motion sickness response (Flanagan et al. 2002). That cannot be the whole story,
however. Motion sickness is an unpleasant experience at the best of times, and that
consideration alone suggests that it would inevitably lead to a state of anticipatory
anxiety or arousal when they are incapable of maintaining a stable posture. This
instability occurs lead to a state of anticipatory anxiety or arousal. I prefer to call
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5 Physiological Mechanisms Underlying Motion Sickness
this a state of arousal because the word “anxiety,” particularly in the minds of many
motion sickness sufferers, conjures up a picture of neurosis or some other mental illness,
which it certainly is not. I wish to stress the normality of this protective response.
5.13
Summary
• The underlying aetiology of motion sickness is still not absolutely clear and
requires further investigation.
• The vestibular overstimulation theory proposes that the vestibular system is the
location of the specialized sense organs which transduce angular and linear
motion stimuli and the absence of the vestibular end-organs results in complete
immunity to motion sickness.
• Changing acceleration acting on the labyrinth in the inner ear is clearly a basic
cause of motion sickness. However, the underlying neurophysiological processes remain unclear.
• The sensory conflict theory proposes that the physiological component is not
simply a single vestibular event, but that it is the body’s response to inharmonious sensory information reaching the comparator in the brain.
• The neural mismatch hypothesis proposes that motion sickness responses are
due to a conflict between the present sensory information and that retained from
the past.
• The heuristic mathematical model associates the incidence and severity of
motion sickness and is related to the magnitude of difference between a vector
that represents all sensory input and one that represents the expectancy of that
information.
• The subjective vertical conflict theory states that motion sickness may be provoked only in conditions where there is a mismatch between the computed
subjective vertical based on the incoming sensory information and the one
computed by the internal model.
• The postural instability theory is based on an ecological concept of the underlying control of orientation, stating that animals experience motion sickness
prior to the onset of the symptoms of motion sickness and is necessary to this
response.
• Treisman’s evolutionary hypothesis suggests 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 visual, vestibular
or proprioceptive inputs are repeatedly and unpredictably perturbed.
• The nystagmus hypothesis proposes that, in a provocative motion environment,
motion sickness would be prevented if the afferent signals from the extra-ocular
muscles were blocked.
• I suggest that the underlying cause of motion sickness is likely to be a combination of these various hypotheses, together with a variable explanation.
References
109
References
Bard P, Woolsey CW, Snider RS, Mountcastle VB, Bromley RB (1947) Delimitation of central
nervous system mechanisms involved in motion sickness. Fed Proc 6:72
Benson AJ (1984) Motion sickness. In: Dix MR, Hood JD (eds) Vertigo. Wiley, Chichester
Benson AJ (1988) Motion sickness. In: Ernsting J, King P (eds) Aviation medicine, 2nd edn.
Butterworth-Heinemann Ltd., Oxford
Bles W (1996) Mechanisms and theory of motion sickness. In: Presented at the AGARD/AMP
short course on prevention and treatment of motion effects in aviation, Fürstenfeldbruck,
Germany, and Lisbon, Portugal, September 1996
Bles W, Bos JE, de Graaf B, Groen E, Wertheim AH (1998) Motion sickness: only one
provocative conflict? Brain Res Bull 47(5):481–487
Brand JJ, Perry WLM (1966) Drugs used in motion sickness. A critical review of the methods
available for the study of drugs of potential value in its treatment and of the information which
has been derived by these methods. Pharmacol Rev 18(1):895–924
Brizzee KR, Neal LM (1954) A reevaluation of the cellular morphology of the area postrema in
view of recent evidence of a chemoreceptive function. J Comp Neurol 100:41
Claremont CA (1931) The psychology of seasickness. Psyche 11:86–90
Coats AC, Norfleet WT (1998) Immersed false vertical room: a new motion sickness model.
J Vestib Res 8(2):135–149
Dichgans J, Brandt T (1973) Optokinetic motion sickness as pseudo-Coriolis effects induced by
moving visual stimuli. Acta Otolaryngologica 76:339–348
Ebenholtz SM (1988) Sources of asthenopia in navy flight simulators. Defense Logistics Agency,
Defense Technical Information Center, Alexandria, VA, Accession Number AD-A212699
Ebenholtz SM, Cohen MM, Linder BJ (1994) The possible role of nystagmus in motion sickness: a
hypothesis. Aviat Space Environ Med 65:1032–1035
Flanagan MB, May JG, Dobie TG (2002) Optokinetic nystagmus, vection and motion sickness.
Aviat Space Environ Med 73:1067–1073
Gay LN (1954) Labyrinthine factors in motion sickness. Int Rec Med General Pract Clin 176
(12):628–630
Graybiel A (1970) Susceptibility to acute motion sickness in blind persons. NAMI1100, Naval
Aerospace Medical Center, Pensacola, FL
Guedry FE (1970) Conflicting sensory orientation cues as a factor in motion sickness. In: 4th
symposium on the role of the vestibular organs in space exploration, Naval Aerospace Medical
Institute, Naval Aerospace Medical Center, September 24–26, 1968, Pensacola, FL. NASA
SP-187, pp, 45–51, Office of Technology Utilization, NASA, Washington, DC
Guedry FE (1991) Motion sickness and its relation to some forms of spatial orientation:
mechanisms and theory. In: Motion sickness: significance in aerospace operations and
prophylaxis, AGARD lecture series 175 (AGARD-LS-175), North Atlantic Treaty
Organization Advisory Group for Aerospace Research and Development, Neuilly-sur-Seine,
France, vol 2, p 1
Held R (1961) Exposure history as a factor in maintaining stability of perception and coordination.
J Nerv Mental Dis 132:26–32
Held R, Mikaelian H (1964) Motor-sensory feedback versus need in adaptation to rearrangement.
Perceptual Motor Skills 18:685–688
Hill J (1936) The care of the sea-sick. Br Med J 2:802–807
Houchin KW, Dunbar JA, Lingua RW (1992) Reduction of postoperative emesis in medial rectus
muscle surgery. Invest Ophthalmol Visual Sci 33:1336
Irwin JA (1881) The pathology of sea-sickness. Lancet 1881(2):907–909
Isaacs B (1957) The influence of head and body positions on the emetic action of apomorphine in
man. Clin Sci 16:215–221
James W (1882) The sense of dizziness in deaf-mutes. Am J Otolaryngol 4:239–254
110
5 Physiological Mechanisms Underlying Motion Sickness
Johnson WH, Mayne JW (1953) Stimulus required to produce motion sickness: restriction of head
movement as a preventative of airsickness—field studies on air borne troops. J Aviat Med 24
(400–411):452
Johnson WH, Stubbs RA, Kelk GF, Franks WR (1951) Stimulus required to produce motion
sickness. 1. Preliminary report dealing with importance of head movements. J Aviat Med
22:365–374
Katz RL, Bigger JT Jr (1970) Cardiac arrhythmias during anesthesia and operation.
Anesthesiology 33:193–213
Kellogg RS, Kennedy RS, Graybiel A (1964) Motion sickness symptomatology of labyrinthine
defective and normal subjects during zero gravity maneuvers. AMRL-TDR-64-47. Aerospace
Medical Research Laboratories, Wright- Patterson Air Force Base
Kennedy RS, Graybiel A, McDonough RC, Beckwith D Jr (1968) Symptomatology under storm
conditions in the North Atlantic in control subjects and in persons with bilateral labyrinthine
defects. Acta Otolaryngologica 66:533–540
Lackner JR, DiZio P (1991) Decreased susceptibility to motion sickness during exposure to visual
inversion in microgravity. Aviat Space Environ Med 62:206–211
Lackner JL, Graybiel A (1981) Variations in gravitoinertial force level affect the gain of the
vestibulo-ocular reflex: implications for the etiology of space motion sickness. Aviat Space
Environ Med 52:154–158
Laffan RJ, Borison HL (1957) Emetic action of nicotine and lobeline. J Pharmacol Exp Therap
121:468–476
Lansberg MP (1960) A primer of space medicine. Elsevier, Amsterdam
Leigh RJ, Daroff RB (1985) Space motion sickness: etiological hypotheses and a proposal for
diagnostic clinical examination. Aviat Space Environ Med 56:469–473
Matsuo V, Cohen B (1984) Vertical optokinetic nystagmus and vestibular nystagmus in the
monkey: up-down asymmetry and effects of gravity. Exp Brain Res 53:197–216
McNally WJ, Stuart EA (1942) Physiology of the labyrinth reviewed in relation to seasickness and
other forms of motion sickness. War Med 2:683
Milot JA, Jacob JL, Blanc VF, Hardy JF (1983) The oculocardiac reflex in strabismus surgery.
Can J Ophthalmol 18:314–317
Minor JL (1896) Seasickness: its cause and relief. N Y Med J 64:522–523
Money KE (1970) Motion sickness. Physiol Rev 50:1–38
Money KE, Cheung BS (1983) Another function of the inner ear: facilitation of the emetic
response to poisons. Aviat Space Environ Med 54(3):208–211
Morales MF (1946) Asynchrony of labyrinthine receptors as a physical factor in motion sickness.
Bull Math Biophys 8:147–157
Norfleet WT, Coats AC, Powell MR (1995) Inverted immersion as a novel gravitoinertial
environment. Aviat Space Environ Med 66:825–828
Oman CM (1990) Motion sickness: a synthesis and evaluation of the sensory conflict theory. Can J
Physiol Pharmacol 68:294–303
Reason JT (1970) Motion sickness: a special case of sensory rearrangement. Adv Sci 26:386–393
Reason JT (1978) Motion sickness adaptation: a neural mismatch model. J Roy Soc Med 71:819–
829
Reason JT, Brand JJ (1975) Motion sickness. Academic Press, New York, NY
Reynolds TT (1884) On the nature and treatment of seasickness. Lancet 123(3174):1161–1162
Riccio GE, Stoffregen TA (1991) An ecological theory of motion sickness and postural instability.
Ecol Psychol 3(3):195–240
Sjöberg AA (1929) Experimental studies of the eliciting mechanism of seasickness. Acta
Otolaryngol 13:343
Steele JE (1970) The symptomatology of motion sickness. In: Proceedings of the fourth
symposium on the role of the vestibular organs in space exploration, NASA, SP-187, p 97
Takahashi M, Saito A, Okada Y, Takei Y, Tomizawa I, Uyama K, Kanzaki J (1991) Locomotion
and motion sickness during horizontally and vertically reversed vision. Aviat Space Environ
Med 62:136–140
References
111
Treisman M (1977) Motion sickness: an evolutionary hypothesis. Science 197:493–495
von Baumgarten RJ, Thumler R (1979) A model for vestibular function in altered gravitational
states. Life Sci Space Res 7:161–170
von Gierke HE, von Parker DE (1994) Differences in otolith and abdominal viscera graviceptor
dynamics: implications for motion sickness and perceived body position. Aviat Space Environ
Med 65:747–751
von Holst E (1954) Relations between the central nervous system and the peripheral organs. Br J
Animal Behav 2:89–94
Wang SC, Borison HL (1950) The vomiting center: a critical experimental analysis. Arch Neurol
Psych 63:928–941
Wang SC, Chinn HI (1954) Experimental motion sickness in dogs: functional importance of
chemoreceptive emetic trigger zone. Am J Physiol 178:111–116
Wang SC, Chinn HI (1956) Experimental sickness in dogs: importance of labyrinth and vestibular
cerebellum. Am J Physiol 185:617
Chapter 6
Psychological Mechanisms That
Exacerbate Motion Sickness
Abstract From the beginning of my research into motion sickness in the military, I
have believed that there must be a psychological component in the aetiology of this
malady. I have based this opinion on the notion that individuals whose careers are
in jeopardy are most likely to have an arousal overlay when confronted with their
provocative motion environment. This is also likely to happen to the majority of
people outside the military if previous motion experiences have been uncomfortable. That does not mean to infer that motion sickness is entirely “psychological.” It
merely suggests that the psychological component, based on memories of previous
motion discomfort and/or the effect that motion sickness may have on future
aspirations, contribute to an individual’s inability to adapt to provocative motion. In
addition, I also believe that the situation is made worse for high achievers, as we
shall see later.
I have already pointed out that there is a psychological component in the aetiology
of motion sickness. There is considerable overlap in the signs and symptoms
characterising motion sickness and those associated with a number of emotional
states. The current view of emotional response emphasises the labelling of such
reactions within the predisposing environmental and social context (Schachter
1971). In addition, the nature and function of these emotional reactions are seen to
have evolved by way of amplifying certain cognitive experiences for the purpose of
storing them more successfully in memory. It is also clear that the tone of voice
communicates an emotional emphasis during social discourse. One view of how
emotions are generally initiated suggests that cognitive or perceptual difference is
often involved (Mandler 1987). This can occur at a cognitive level in which
expectation is breached (e.g., inappropriate social behaviour), but also at a less
conscious level where intention is frustrated (e.g., stumbling in a precarious situation). Thus, novelty, discrepancy, and interruption are seen to be causative triggers
for visceral reactions (e.g., excitement, anger, or fear). In this context, for example,
the types of emotions that are experienced on amusement park rides depend upon
the cognitive attitude of the participants, which in turn is related to the immediate
company, general frame of mind and past experiences. Some may feel elated, while
others experience fear, in these types of situations that usually disturb an individual’s expectations of whole body motion. As already described, motion sickness is
© Springer Nature Switzerland AG 2019
T. G. Dobie, Motion Sickness, Springer Series on Naval Architecture,
Marine Engineering, Shipbuilding and Shipping 6,
https://doi.org/10.1007/978-3-319-97493-4_6
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6 Psychological Mechanisms That Exacerbate Motion Sickness
thought to stem from a neural mismatch, which is a very basic form of perceptual
conflict. It may be that the same mechanisms that underlie a person’s fundamental
emotional response also account for motion sickness. The major difference in
motion settings being that there is a relatively slower development of visceral
reactions and in turn, the cognitive interpretations of these sensations. Most would
agree, however, that there is an emotional reaction involved in the motion sickness
response.
I very much agree with Wendt (1948) who has stated that no absolute distinction
can be made between psychological and physiological factors when discussing
motion sickness. He also believed that when people referred to psychological
factors in the causation of motion sickness, they were usually referring to one or
more of the following seven fairly distinct classes of factors:
In Wendt’s words:
1. Expectation and suggestion. What the traveller has heard about airsickness, the attitude
he sees others adopt, the observed effects of rough air on others, and his expectations
from his own past experience affect liability to sickness.
2. The specific conditioning effects of past experience. Sickness in autos, boats, amusement park devices, or aeroplanes tends to condition nausea to whatever stimuli were
present at the time. These include sights, sounds, odours, and, most important, the
stimuli from motion itself.
3. The specific habituation effects of past experiences. Experience ordinarily lessens
susceptibility by eliminating the unexpected, leading to a more correct estimate of the
chances of sickness, and by setting up some barrier against elicitation of nausea such as
occurs whenever stimuli are repeated.
4. The effects of concurrent activity. Aeroplane pilots and automobile drivers infrequently
get sick; navigators and passengers more often do. No helpful explanation of this has
been proposed but it appears to be well authenticated that the nature of one’s activity
can have a considerable effect on proneness to sickness.
5. The effects of concurrent emotional state. Apprehension, fear, anxiety and grief are
often present when passengers become airsick. Opposing emotional states of confidence, satisfaction and well-being are regarded as preventing sickness.
6. Airsickness may be a motivated symptom which frees a student by wash-out from a
situation which he wishes to escape
7. Airsickness may be a weakness associated with certain personality types, e.g., anxiety
neurotics, who are more susceptible to the effects of the psychological factors involved
in flying.
I am bound to say that I have mixed feelings about this list. In terms of the first 3
factors, in general I would agree that past experience is a potent factor in the way
that an individual approaches a provocative motion environment. As we shall see in
a moment, uncomfortable past experiences can create an anticipatory arousal on
reentering a provocative motion environment. Positive habituation effects arising
from positive pleasant experiences on motion devices prevent arousal and allow
adaptation to occur optimally. Regarding factor 4, a pilot or driver has a number of
advantages over a passenger. His or her head movements are likely to be fewer and
the mind more focused; features that are likely to reduce motion sickness. It is
difficult to comment on factor 5 other than to refer to the comments I have already
6 Psychological Mechanisms That Exacerbate Motion Sickness
115
made with regard to past experiences. In terms of factor 6, I have certainly come
across situations like this. As for factor 7, I must say that it has not been my
experience that “weakness associated with certain personality types” plays a
prominent role in severe motion sickness. On the contrary, as we shall see later
when discussing cognitive-behavioural training in Chap. 12, those with so-called
“intractable airsickness” who were successfully returned to unrestricted flying
tended to be high achievers.
6.1
Arousal
It is natural to develop a form of anxiety due to feelings of discomfort or nausea
brought about by certain provocative manoeuvres, or when exposed to a different
and unfamiliar mode of travel. This is due to the arousal that typically develops
when one is exposed to situations known to be uncomfortable or threatening. The
magnitude of this arousal is also likely to be determined by an individual’s personality. Perhaps people who seem prone to motion sickness are somewhat more
introspective and more responsive to environmental changes than those individuals
who are apparently less prone to motion sickness. Personality differences may
determine how an individual reacts to these motion discomforts in terms of anticipation and/or severity of response. This does not in any way imply that motion
sickness is a neurotic response on the part of that individual. On the contrary, this is
seen as a perfectly normal and understandable “protective” response. Indeed, RAF
flight trainees who have been successfully treated for apparently intractable motion
sickness appeared to be high achievers who performed well on their return to full
flight status (Dobie 1974). What is abnormal in this situation is not the subjective
response, but rather the provocative motion environment. Unlike the child withdrawing its hand from a flame, which carries no ensuing penalty, the protective
motion sickness responses can be a nuisance to live with, perhaps for a lifetime.
These responses can and do limit an individual’s professional and social life, factors
which are likely to further exaggerate the degree of anxiety. In this context, Wendt
points out that he does not find any reference to airsickness or seasickness as a
symptom of combat neurosis. In his opinion, “If anxiety is the main cause of motion
sickness, all cases of combat neurosis should suffer from chronic motion sickness.”
Schwab (1954) has described four common causes of motion sickness, “in
addition to the disturbances from labyrinthine stimulation.” The first and second of
these consist of smell and vision which stimulate the senses. He has suggested that,
in themselves they are not enough to provoke sickness, but in combination with
labyrinthine stimulation they become a frequent cause of disability. The third,
which we are presently reviewing, is psychogenic. He is of the opinion that this sort
of stimulus results from both anticipation of the journey or simply conditioning
from past experiences. The past experiences, if unpleasant, likely to create a state of
arousal prior to subsequent exposures in similar situations. The fourth, a more
specific group, included increased arousal in females throughout the menstrual
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6 Psychological Mechanisms That Exacerbate Motion Sickness
cycle and persons with either a peptic or duodenal ulcer. I agree that this question of
anticipatory arousal plays a large part in the aetiology of motion sickness. It is also
interesting to note that hormonal causes are presently being examined as the reason
for the higher incidence of motion sickness in women compared to men, age for
age, as previously discussed in Chap. 3.
The main differences in the incidence of motion sickness among individuals
exposed to identical motion stimuli could be physiological. I believe, however, that
it is more likely to be due to the personal responses that different individuals have
previously experienced in these provocative motion environments, and how they
have reacted to them. These include practice, attitude of mind, and levels of mental
arousal. On the one hand, certain passengers have been known to report that they
feel motion sick before the ship even leaves the dock. Others claim that they never
get sick at sea “whatever the weather,” but on the other hand, may state that they
cannot cope with the movements of fairground devices or other forms of
provocative motion. There are indeed many seeming anomalies in individual histories. Schwab points out that many of the older articles in the literature on the
subject of seasickness describe motion susceptible or nervous individuals who go to
bed on a ship while it is still tied up at the dock and soon become very ill, even
though the ship has not yet sailed. He has labelled this a simple anxiety related to
the anticipation of motion. He has also pointed out that there have been numerous
well documented cases of individuals who, although suffering from motion sickness, have “recovered promptly under a stimulus associated with danger, combat, or
increased responsibility and interest.” Nieuwenhuijsen (1958) observed that the
only time Lord Nelson was free of seasickness was when he entered battle. These
probably represent examples of the powerful protection afforded by distraction.
This subject is emphasised later when I review various examples of the advantage
of cognitive protection in stressful situations (Chap. 14).
Wendt (1948), as previously stated, had not found any reference to airsickness or
seasickness as a symptom of combat neurosis. In similar vein, Birren and Fisher
(1947) have observed that the incidence of seasickness shows absolutely no relationship to passengers’ fear of drowning or other major disaster on board a
ship. Zwerling (1947) attempted the first experiment to investigate the role of fear in
the aetiology of motion sickness. He administered electric shocks to volunteers
while they were tilting their heads in the frontal plane during spinning in a rotating
chair. He reported that shocked subjects suffered more motion sickness than the
unshocked subjects. The criterion for indicating a motion sickness response has
been the subject’s request to stop the rotation after an interval of less than 12 min.
However, as Birren has pointed out in 1949: “This criterion of sickness is complicated by the fact that an electric shock is an annoyance by itself, and individuals
may have requested that the motion be stopped not only because they felt ill, but
they wished to avoid further shocks.”
Birren did, however, make the interesting observation that there was no apparent
relationship between a subject’s neurotic tendencies and susceptibility to sickness
on the rotating chair. He has concluded: “Within the limitations of the study, it
6.1 Arousal
117
would appear that, if fear is an important factor, it operates independently of
neurotic personality qualities.”
Reason and Brand (1975) have reviewed this possible association between fear
and anxiety and motion sickness and came to the conclusion that “these factors are
only of secondary importance.” However, that is not altogether the end of the story
because fear and anxiety can be invoked by quite different but equally important
personal triggers. For example, my study of the RAF flight trainees, previously
reported, would suggest that the anxiety or arousal has not necessarily been exocentric, rather it has been internal or egocentric, and highly provocative to high
achievers who have been confronted with a problem that promised to ruin their
future. Who knows what levels of arousal are created in these individuals when they
are about to be exposed to conditions that affect their long held plans? It is interesting to relate an observation made by Reinhardt (1964) who reported that the term
“emotion sickness” had been coined by the Head of the Division of
Neuropsychiatry at the US Naval School of Aviation Medicine, to describe types of
airsickness seen in flight students. By way of example, he has mentioned that some
cannot stomach the “invisible instructor” in the rear cockpit who was, it seems, ever
ready with quick and often biting criticism. He also referred to the fear of carrying
out newly learned procedures, or the positional uncertainty of certain aerial
manoeuvres. In that context he believed that emotional stress was an indispensable
condition for airsickness.
6.2
Personality Factors
Collins and Lentz (1977) have noted that earlier conceptions of motion sickness
sufferers as being of weak constitution and generally lacking in “moral fibre” are
remarkable since, as I have already stated in Chap. 1, numerous courageous people,
such as Julius Caesar, Admiral Lord Nelson (and many of his fellow admirals), and
Lawrence of Arabia all suffered from chronic motion sickness. Collins and Lentz
have conducted a comprehensive investigation of the relationship between motion
sickness susceptibility and selected personality factors, by comparing those subjects
who have reported high susceptibility with those who deny any such susceptibility.
They studied four groups of college students, with 37 subjects in each of the
following groups: motion sickness susceptible males, motion sickness susceptible
females, non-susceptible males, and non-susceptible females. An assessment of
susceptibility to motion sickness has been based on scores obtained from a modified
version of the motion sickness questionnaire used by Birren (1947). The questionnaire was administered to 2,432 students and only those with extreme scores
had been included in the study. Within the susceptible and non-susceptible categories, the subjects were selected at random. Each subject was tested on at least
three, but not more than six, of the eight tests that had been chosen for the study.
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6 Psychological Mechanisms That Exacerbate Motion Sickness
The tests and results obtained were as follows:
1. Floor Ataxia Test Battery: This has been reported to be an indicator of loss or
impairment of vestibular function. Males had significantly better balance scores
than females. This has been attributed to differences between the
non-susceptible men and women (Fregly and Graybiel 1968).
2. State-Trait Anxiety Inventory: This was developed by Speilberger and his
associates as a means of assessing anxiety characteristics. Susceptible individuals had significantly higher trait-anxiety scores than non-susceptibles, indicating that two relatively permanent personality characteristics, trait anxiety and
motion sickness susceptibility, were associated either directly or indirectly. The
“state” portion of the inventory was administered both before and after rotatory
vestibular stimulation. Before rotation, there were no significant state anxiety
differences between the groups. Following rotation, however, susceptible individuals had significantly higher anxiety scores (Spielberger et al. 1970). This is
not really surprising since susceptible individuals had a heightened state of
arousal and one would expect them to feel more anxious after a period of
exposure to provocative motion.
3. Menstrual Distress Questionnaire (Form A): This has been constructed to
determine the extent to which women experienced common menstrual symptoms. Of the 47 symptoms possibly related to menstrual distress, only fatigue
was expressed differently in that susceptible women reported more fatigue.
When the 47 symptoms had been collated to the suggested eight general factors,
however, there were no significant differences between susceptible and
non-susceptible women (Moos 1969).
4. Cornell Medical Index: This health questionnaire was designed to collect general medical and psychiatric data to facilitate patient examination. Susceptible
subjects and women had significantly more “yes” answers (Brodman et al.
1949).
5. Cornell Word Form: This form was designed to screen for potentially serious
neuropsychiatric and psychosomatic disturbances. Motion sick susceptible
individuals had significantly higher scores; there were no significant differences
based on sex (Buros 1974).
6. Eysenck Personality Inventory: This has been designed to measure personality
in terms of extroversion-introversion and neuroticism-stability. Non-susceptible
subjects had significantly higher scores on the extroversion scale. In addition,
higher extroversion scores for non-susceptibles were primarily a factor of the
difference between susceptible and non-susceptible males. On the neuroticism
scale, susceptibles had significantly higher scores (Eysenck and Eysenck 1968).
7. Rotter Internal-External Locus of Control Scale: This was developed to assess
the extent to which individuals believed that they could control or influence
events that affect them. This scale did not significantly identify any of the groups
in the study (Rotter 1966).
6.2 Personality Factors
119
8. The 16 Personality Factors Test (Form A): This is a multi-dimensional personality factor questionnaire. All primary, secondary, and criterion scores fell
within 1 S.D. of the mean that has been established for a college student population (Cattell et al. 1970).
Collins and Lentz reported that, in general, “non-susceptibles tended to score as
less neurotic, better adjusted, and more venturesome than susceptibles, and susceptibles in general had factors in common with women (tender-minded, subjective).” Having said that, they concluded that although there were apparently some
clear psychological differences between individuals at the extremes of the range of
susceptibility to motion sickness, rather than indicating the basis for motion sickness, they were probably best regarded as correlates of population extremes, for the
following reasons. First, motion sickness can be induced in so-called
non-susceptible persons. Second, the incidence of motion sickness varies with
age, as has already been described. Third, not all people who are described as
masculine, extroverted, and low in general anxiety are found to be non-susceptible.
Finally, the researchers suggested the possibility that non-susceptibles were not
different from those considered to be susceptible in terms of the personality characteristics applied in this study.
Collins and Lentz concluded that their results were probably less of an indication
of a personality continuum with regard to a person’s susceptibility to motion
sickness than a description of the personality characteristics of those who were
likely to be sick in almost any motion environment. As we shall see, Mirabile
(1990) has pointed out the importance of employing representative samples for
study.
Keinan et al. (1981) reported on two studies that they have carried out concerning the relationship of certain personality types and the quality of those subjects’ performance when exposed to provocative motion. In the first study, they
evaluated the validity of various predictors of quality of performance under conditions of provocative motion and from their results they produced a prediction
formula. In the follow-up study they evaluated the predictive value of that formula.
The personality tests that they had chosen were “Locus of Control” (LOC),
Rotter (1966, 1975) and the “repression-sensitisation” (R-S) scale, Byrne (1961),
Byrne et al. (1963). Rotter has characterised people with an external locus of
control as having a general tendency to believe that external, uncontrollable forces
would determine their fate. These people have little confidence in being able to
reduce the effects of these forces. On the other hand, those with an internal locus of
control tended to trust their own ability to determine their fate and have a relatively
high degree of self-esteem and confidence. In terms of Byrne’s R-S Scale, “repressors” generally failed to prepare themselves to face continuous stress, whereas
“sensitisers” tended to recognise stress and responded rapidly.
Keinan et al. concluded that their diverse predictors varied considerably in their
effectiveness and that the biographical inventory was the most powerful of those
tested (Kennedy and Graybiel 1965). As far as personality characteristics were
concerned, however, they reported that they had been somewhat disappointed in the
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results. Nevertheless, they found an important difference in their effectiveness as
predictors. They reported that the LOC scale had a correlation with performance
that was practically zero. Keinan et al. suggested that this either meant that the
assumed difference between people who were internally or externally oriented, in
terms of their ability to cope with motion symptoms, was not valid, or that the
Rotter scale was not a valid measure of locus of control. On the other hand, the
correlation between R-S and performance offered some support for the assumed
relationship between these variables.
Siem and Murray (1994) felt that the research literature generally suggested that
personality variables contributed little to pilot performance. They suggested that
one reason for not finding stronger links might be the “lack of appropriate taxonomies for both personality constructs and for performance constructs.” Siem and
Murray examined the relationship between various personality factors and combat
performance using the so-called “Big Five” model of personality developed by
Goldberg (1992), namely (1) extraversion, (2) agreeableness, (3) conscientiousness,
(4) emotional stability, (5) culture (openness to experience) and a multi-component
model of pilot combat performance.
In this study, ten USAF pilots rated the importance of 60 traits for effective
performance of such capabilities as flying skills and crew management. Their
responses pointed to the fact that pilots with different aircraft backgrounds all
agreed that the personality trait that was the most important measure of performance
overall was “conscientiousness.” This result has interesting implications in terms of
the cognitive-behavioural anti-motion sickness training programme. I found that the
high achiever was likely to be more profoundly affected by the implications of
being motion sick than the individual who was less dedicated to his task. At the
same time, the conscientious client performed better in the desensitisation training
programme and, as a group, these clients tended to be above the average in terms of
their future performance, as I shall discuss later. It is very interesting to note that
Admiral Zumwalt Jr. was extremely motion sick as an ensign (Stillwell 1976).
6.3
Measured Stress Responses
Kohl (1985) has pointed out that he and co-workers (La Rochelle et al. 1982)
reported previously that motion sickness led to an increase in the level of
adrenocorticotropic hormone (ACTH), cortisol, epinephrine, and norepinephrine,
but failed to show any change in the level of thyroid-stimulating hormone (TSH),
indicating a general stress response to provocative motion stimulation. Since hormonal responses might have some kind of an adaptive role in helping individuals to
better deal with provocative motion, they measured base levels of various hormones
before and after these individuals had been exposed to provocative motion, or the
administration of anti-motion sickness medication. In this study, anti-motion
sickness drugs had been given to both susceptible and non-susceptible subjects
before they were exposed to a Coriolis Sickness Susceptibility Index (CSSI) test
6.3 Measured Stress Responses
121
(see Chap. 8) to induce motion sickness through stressful cross-coupled (Coriolis)
acceleration. They found that the non-susceptible group of subjects showed greater
increases in ACTH, epinephrine, and norepinephrine after provocative motion.
Pre-drug levels of ACTH were higher in non-susceptible subjects. Acute pharmacological blocking of hormone responses to provocative motion or changes in the
levels of ACTH, have not correlated with individual susceptibility to motion
sickness, nor had they found any correlation between epinephrine and the release of
ACTH.
In Kohl’s opinion, the differences shown by these endocrines might have represented “neurochemical markers” that indicated susceptibility to provocative
motion, stress, or general adaptability. He further suggested that longer-term
adjustment of the levels of these hormones might provide a more effective approach
to preventing motion sickness than acutely blocking or stimulating particular
receptors. He opined that those individuals who have exhibited a lower susceptibility to provocative motion were more adaptable to environmental stressors or
sensory conflicts because they possessed higher baseline levels, or activity, of
certain specific endocrine components such as corticotropic releasing factor and
adrenocorticotropic hormone, or because their endocrine systems were capable of
showing greater responsiveness. In that case, these individuals might have possessed the innate ability “to interpret and resolve environmental stresses and sensory conflicts more rapidly.”
Stalla et al. (1985) evaluated 11 steroid hormones to see if various levels of
stress caused different hormonal responses and whether these, in turn, might help to
grade the severity of motion sickness objectively. The 11 adrenal hormones selected
for this comprehensive investigation were aldosterone, corticosterone, 11deoxycorticosterone, progesterone, 17-OH progesterone, 11-deoxycortisol, cortisol, cortisone, testosterone, androstenedione, and dehydroepiandrosterone sulphate.
From a total of 34 military personnel, aged between 20 and 30 years, they selected
15 subjects based on the severity of their motion sickness histories and subdivided
them into three groups of 5 subjects each, on the following basis: highly sensitive,
medium sensitivity and poorly or non-sensitive to provocative motion. This sensitivity level was based upon the blindfolded subject’s motion sickness response to
active upper body movements while being rotated in a Bárány chair at 72°/s. In
addition, motion sickness symptoms were recorded by questionnaire every 2 min
and scored according to Miller and Graybiel’s (1970) grading system (Table 6.1).
Sensitivity to motion sickness was rated as “high” if the subject tolerated less than
12 min of rotation; “medium” when the duration lay between 20 and 30 min and
demonstrated more than 12 motion sickness points and non-sensitive if the duration
was greater than 30 min and the number of motion sickness points less than 13.
Motion sickness was induced by means of cross-coupled (Coriolis) stimulation on a
rotating chair. Severe motion sickness occurred after both a short period of rotation
and mild motion sickness following 30 min of rotation, as have small hormonal
changes. These researchers found that if the duration of rotation has been taken into
account, androstenedione and 11 deoxycortisol appeared to be sensitive indicators
of motion sickness. When pronounced malaise was experienced after a long period
122
6 Psychological Mechanisms That Exacerbate Motion Sickness
Table 6.1 Diagnostic categorization of different levels of severity of acute motion sickness
Category
Pathognomonic
16 points
Major 8
points
Minor 8
points
Minimal 2
points
AQSa 1 point
Nausea
syndrome
Skin color
Vomiting or
retching
Nausea
II, IIIb
Pallor
III
Nausea
I
Pallor II
Epigastric
discomfort
Pallor I
Epigastric
awareness
Flushing/
subjective
warmth II
Cold
III
II
sweating
Increased
III
II
salivation
Drowsiness
III
II
Pain
Central
nervous
system
Levels of severity identified by total points scored:
Frank sickness (FS) > 16 points
Severe malaise (M III) 8–15 points
Moderate malaise A (M IIA) 5–7 points
Moderate malaise B (M IIB) 3–4 points
Slight malaise (M I) 1–2 points
AQSa = additional qualifying symptoms
b
III = severe or marked; II = moderate; I = slight
I
I
I
Headache II
Dizziness—Eyes
closed II Eyes
open III
of rotational stress (24.6 min), a significant increase of all hormones except progesterone, cortisone, testosterone, and dehydroepiandrosterone sulphate has been
observed. Changes in the concentration of plasma aldosterone appeared to correlate
with time only. Stalla et al. concluded that the hormone responses to provocative
motion shown by deoxycortisol and androstenedione might have reflected the
severity of motion sickness even if the duration of exposure had been short. On the
other hand, corticosterone and 11-deoxycorticosterone, progesterone and
17-OH-progesterone only responded in circumstances that involved prolonged
motion stress.
6.4
Relationship of Salivary Gland Function
to Personality and Motion Sickness
Many studies have attempted to relate salivary gland function to various psychopathologic states or to normal personality traits (Costa et al. 1980). Introversion
has been found to be positively correlated with increases in salivation in response to
gustatory stimulation (Corcoran 1964; Eysenck and Eysenck 1967). Gordon et al.
6.4 Relationship of Salivary Gland Function to Personality and Motion Sickness
123
(1992a, b) have compared the salivary flow rate and composition of two groups of
31 subjects, with one group at each end of the scale representing susceptibility to
seasickness. They found no significant differences between these two extreme
groups in terms of either flow rates or electrolyte concentrations of whole saliva in
resting and stimulated states. However, they noted that the amylase activity and rate
of secretion in resting saliva were significantly higher in those subjects susceptible
to seasickness. Gordon et al. also found that the rate of secretion of total protein in
the resting saliva was significantly higher in the group of subjects who were susceptible to seasickness. These workers concluded that their findings could be
explained in terms of higher sympathetic tone in subjects susceptible to seasickness.
Also, salivary amylase levels might be recommended as an additional indicator of
susceptibility to seasickness.
Gordon et al. failed to reproduce the correlation between salivary flow and
motion sickness susceptibility when they measured salivation in subjects at the two
extremes of the motion sickness susceptibility scale. Nevertheless, they did consider
that their method of collecting stimulated saliva, namely, 10 min of spitting whole
saliva with gustatory stimulation every 30 s, has probably produced stronger
stimulation than the techniques employed by Corcoran (1964) and by Eysenck and
Eysenck (1967). In a population of 390 normal subjects, Costa et al. (1980) reported
a significant positive correlation between stimulated parotid saliva flow rate and
four personality traits: namely, introversion; anxiety; conscientiousness and
shrewdness.
Gordon et al. (1994) have further investigated the possible relationship between
motion sickness susceptibility, personality factors, and salivary characteristics.
They measured various personality factors, as evaluated by the Eysenck Personality
Questionnaire (Eysenck and Eysenck 1975), salivary composition and flow in a
group of 29 subjects who were highly susceptible to seasickness and in a control
group of 25 non-susceptible subjects. The control group demonstrated significantly
higher psychoticism scores and significantly lower levels of salivary amylase as
compared to the subjects who were highly susceptible to motion sickness. In
addition, the psychoticism score was positively correlated with the absolute and
relative increase in salivary flow in response to taste stimulation using citric acid.
These researchers pointed out that the psychoticism trait of the Eysenck Personality
Questionnaire has not previously been evaluated in relation to salivary secretion,
and suggested that their findings provided more data in support of the connection
between normal personality traits and salivation.
Gordon et al. (1994) concluded, “the motion sickness syndrome is a complex
integration of responses from a multiple physiological system, also influenced by
normal personality factors.” They believed that the outcome of their study supported the idea that these multiple variables and their relationship called for further
evaluation so as to get a better understanding of the many unknown features of
motion sickness. These views of Gordon et al. have been similar to those put
forward later by May and myself in our monograph (Dobie and May 1994).
In their review of the motion sickness literature, Tyler and Bard (1949) concluded that neither psychological nor psychopathological factors were important in
124
6 Psychological Mechanisms That Exacerbate Motion Sickness
the causation of motion sickness. In addition, Reason and Brand (1975) opined that
there was not likely to be a causal relationship between neuroticism and motion
sickness, but some relationship did seem to exist, however small.
As we shall see later, however, flight trainees who had been grounded because of
intractable airsickness were successfully returned to flying after being managed by
means of my cognitive-behavioural training programme (Dobie 1974). A long-term
follow-up indicated that these subjects were above the average in their efforts to
succeed and perhaps we were seeing features of high achievers in this population. It
might also have been the case that the effects and memories of provocative motion
had induced greater states of arousal in this type of individual than in others.
Mirabile (1990) has summarised what he believed to have been the most
compelling arguments that run counter to a psychological explanation for the
occurrence of motion sickness. First, that motion sickness did not occur during
constant motion, only during acceleration. Second, that by reducing head movements, one could ameliorate symptoms. Third, other sensory systems provided
information about bodily movement, yet motion sickness did not occur when the
vestibular system had been destroyed. Fourth, the greatest degrees of emotional
disturbance have been found in those persons who were classified as having
intermediate, rather than extreme, degrees of sensitivity to provocative motion. In
addition, a greater number of motion resistant, rather than motion sensitive, individuals have been found among psychiatric patients. Finally, Mirabile has observed
that many forms of animals are susceptible to motion sickness, and he thought it
unlikely that emotional factors played a significant part in these less complicated
forms of life.
6.5
Theoretical Considerations
In summary, the underlying cause of motion sickness is likely to be a combination
of physiological factors that create sensory mismatches, together with experiential
anxiety caused by that individual’s attitudes, memories, and past experiences with
motion stimuli. A diagrammatic representation of Dobie and May’s
psycho-physiological model of motion sickness, based on Benson’s physiological
model (1988), together with our added psychological factors (shaded area), is
shown in Fig. 6.1 (Dobie et al. 1989).
When individuals are first exposed to provocative motion, it is reasonable to
assume that a motion sickness response would be “physiological” in origin, because
they are then naive in terms of experience with provocative motion. As they have
disagreeable experiences with motion, however, their arousal grows and the psychological component becomes more significant. The degrees of arousal may also
be affected by a person’s experiences with a variety of different provocative stimuli.
For example, some individuals may have more anticipatory arousal if their experiences with all forms of motion have been unpleasant, however mild.
6.5 Theoretical Considerations
125
Fig. 6.1 A schematic of Dobie and May’s psychophysiological model of motion sickness based
on Benson’s physiological model (Fig. 5.1)
On the other hand, an isolated, more severe exposure may affect the individual’s
expectations less if all other provocative motion experiences have produced no ill
effects. At the same time, the magnitude and importance of that psychological
component is likely to be a reflection of that subject’s personality. I shall discuss
my psychophysiological concept of motion sensitivity further in Chap. 12, where I
propose that anticipatory arousal has an adverse effect on an individual’s ability to
adapt to provocative motion. Such a “multi-layered” concept of the aetiology of
motion sickness does not conflict with Mirabile’s (1990) summary of compelling
arguments against a psychological explanation for the occurrence of motion sickness. The psychological issues are seen as a potentially important component which
can have particularly significant consequences in many people and particularly so in
terms of the management of their motion sickness.
6.6
Summary
• Motion sickness is a psychophysiological response to provocative motion.
• In addition to the physiological causes of motion sickness, anticipatory arousal
caused by previous motion discomfort inhibits adaptation to provocative
motion.
126
6 Psychological Mechanisms That Exacerbate Motion Sickness
• The magnitude of arousal due to feelings of discomfort or nausea brought about
by provocative motion is determined in great measure by an individual’s personality and past experiences.
• Salivary gland function tests have shown that individuals who are susceptible to
seasickness show a significantly higher secretion of total protein in the resting
saliva than those who don’t suffer from this malady. Also, the salivary amylase
levels and rate of secretion are higher in susceptible individuals.
References
Benson AJ (1988) Motion sickness. In: Ernsting J, King P (eds) Aviation medicine, 2nd edn.
Butterworth-Heinemann Ltd., Oxford
Birren JE (1947) Psychophysiological studies of motion sickness. Dissertation. Northwestern
University, Evanston, IL
Birren JE, Fisher MB (1947) Susceptibility to seasickness: a questionnaire approach. J Appl
Physiol 31:288–297
Brodman K, Erdman AJ Jr, Wolff HG (1949) Cornell medical index health questionnaire—
manual. Cornell University Medical College, New York, NY
Buros OK (1974) Tests in print II: an index to tests, test reviews, and the literature on specific tests.
Gryphon Press, II, New Jersey
Byrne D (1961) The repression-sensitization scale: rationale, reliability and validity. J Pers
29:334–349
Byrne D, Barry J, Nelson D (1963) Relation of the revised repression-sensitization scale to
measures of self-description. Psychol Rep 13:323
Cattell RB, Eber HW, Tatsuoka MM (1970) Handbook for the sixteen personality factor
questionnaire (16PF). Institute for Personality and Ability Testing, Champaign, IL
Collins WE, Lentz JM (1977) Some psychological correlates of motion sickness susceptibility.
Aviat Space Environ Med 48(7):587–594
Corcoran DW (1964) The relationship between introversion and salivation. J Psychol 77:298–300
Costa PT Jr, Chauncy HH, Rose CL, Kapur KK (1980) Relationship of parotid salivaflow and
composition with personality traits in healthy men. Oral Surg Oral Med Oral Pathol 50:416–
422
Dobie TG (1974) Airsickness in aircrew. AGARDOGRAPH No. 177, North Atlantic Treaty
Organization Advisory Group for Aerospace Research and Development, Neuilly-sur-Seine,
France
Dobie TG, May JG (1994) Cognitive-behavioral management of motion sickness. Aviat Space
Environ Med 65:C1–C20
Dobie TG, May JG, Fisher WD, Bologna NB (1989) An evaluation of cognitive-behavioral
therapy for training resistance to visually-induced motion sickness. Aviat Space Environ Med
60:307–314
Eysenck SBJ, Eysenck HJ (1967) Salivary response to lemon juice as a measure of introversion.
Percept Mot Skills 24:1047–1053
Eysenck HJ, Eysenck SBG (1968) Eysenck personality inventory—manual. Educ Industr Test
Serv, San Diego
Eysenck HJ, Eysenck SBG (1975) Manual of the eysenck personality questionnaire. Hodder
Stoughton, London
Fregly AR, Graybiel A (1968) An ataxia test battery not requiring rails. Aerosp Med 1968
(39):277–282
References
127
Goldberg LR (1992) The development of markers of the big-five factor structure. Psychol Assess
1992(4):26–42
Gordon CR, Ben-Aryeh H, Spitzer O, Doweck I, Gonen A, Melamed Y, Shupak A (1994)
Seasickness susceptibility, personality factors and salivation. Aviat Space Environ Med
65:610–614
Gordon CR, Jackman Y, Ben-Aryeh H, Doweck I, Spitzer O, Szargel R, Shupak A (1992a)
Salivary secretion and seasickness susceptibility. Aviat Space Environ Med 63:356–359
Gordon CR, Spitzer O, Shupak A, Doweck H (1992b) Survey of mal de debarquement. BMJ
304:544
Keinan G, Friedland N, Yitzhaky J, Moran A (1981) Biographical, physiological and personality
variables as predictors of performance under sickness-inducing motion. J Appl Psychol 66
(2):233–241
Kennedy RS, Graybiel A (1965) The dial test: a standardized procedure for the experimental
production of motion sickness symptomatology in a rotating environment. NSAM 930, NASA
Ord. No. R-93, Naval School of Aviation Medicine, Pensacola FL
Kohl RL (1985) Endocrine correlates of susceptibility to motion sickness. Aviat Space Environ
Med 56:1158–1165
La Rochelle FT Jr, Leach CS, Homick JL, Kohl RL (1982) Endocrine changes during motion
sickness: effects of drug therapy. In: Reprints of the Aerospace Medical Association Annual
Scientific Meeting. Washington, DC: Aerospace Medical Association
Mandler GW (1987) Emotion. In: Gregory RL (ed) The Oxford companion to the mind. Oxford
University Press, New York, NY
Miller EF, Graybiel A (1970) A provocative test for grading susceptibility to motion sickness
yielding a single numerical score. Acta Oto-laryngologica 274:5
Mirabile CS Jr (1990) Motion sickness susceptibility and behavior. In: Crampton GH (ed) Motion
and space sickness. CRC Press, Boca Raton, FL
Moos RH (1969) Menstrual distress questionnaire: preliminary manual. Stanford University
School of Medicine, Stanford, CA
Nieuwenhuijsen JH (1958) Experimental investigations on seasickness. Ph.D. Thesis. University
of Utrecht, The Netherlands
Reason JT, Brand JJ (1975) Motion sickness. Academic Press, New York, NY
Reinhardt RF (1964) The many faces of airsickness. Flight Safety Newsletter. No. 964, US Naval
School of Aviation Medicine, Pensacola, FL
Rotter JB (1966) General expectancies for internal versus external control and reinforcement.
Psychol Monogr 80(1):1–28
Rotter JB (1975) Some problems and misconceptions related to the construct of internal versus
external control of reinforcement. J Consult Clin Psychol 43:56–67
Schachter S (1971) Emotion, obesity and crime. Academic Press, New York, NY
Schwab RS (1954) The nonlabyrinthine causes of motion sickness. Int Record Med Gen Pract Clin
167(12):631–637
Siem FM, Murray MW (1994) Personality factors affecting pilot combat performance: a
preliminary investigation. Aviat Space Environ Med 65(5):A45–A48
Spielberger CD, Gorsuch RL, Lushene RE (1970) STAI manual for the state-trait anxiety
inventory. Consulting Psychologists Press, Palo Alto, CA
Stalla GK, Doerr HG, Bidlingmaier F, Sippel WG, Von Restorff W (1985) Serum levels of eleven
steroid hormones following motion sickness. Aviat Space Environ Med 56:995–999
Tyler DB, Bard P (1949) Motion sickness. Physiol Rev 29:311–369
Wendt GR (1948) Of what importance are psychological factors in motion sickness? J Aviat Med
19:24–33
Zwerling I (1947) Psychological factors in susceptibility to motion sickness. J Psychol 23:219–239
Zumwalt ER (1976) On watch: a memoir. New York: Quadrangle/New York Times Book Co
(quotations from Stillwell P)
Chapter 7
Adaptation to Provocative Motion
Abstract The question of adaptation is a key issue in dealing with motion sickness. It is generally accepted that most people should be capable of adapting to
provocative motion. In that case, why do so many people suffer from chronic
motion sickness? As I have said in the previous chapter, I believe that this is due to
a psychological component based upon unpleasant motion responses in the past;
perhaps as a result of individual motion experiences from a young age. Early and
continued exposure to provocative motion may either sensitise a person or allow
that person to adapt. This will depend upon the duration, character and frequency of
exposure to whatever form of motion. In a sense it may be entirely fortuitous and
depend on social and/or geographical circumstances. I shall return to this question
later in Chap. 12, when discussing cognitive-behavioural training.
Apart from being highly selective, the body’s sensory systems are specifically
designed to respond to a constant stimulus by adapting, or decreasing, their
response. Money (1970) has discussed the issues of adaptation and habituation in
his review of motion sickness. He has suggested that the word “adaptation” seemed
to be used to describe three events: first, a changing response to stimuli and in
particular, a reduction; second, the changing mechanism within the body that has
been responsible for that “response decline;” and third, the acquisition of these
changes. He described “habituation” as the process of “acquiring the adaptive
change and the decrease in response.” In the context of motion sickness, it has been
estimated that some 95% of all persons susceptible to motion sickness have the
capability of adapting to provocative motion. Although this figure has been commonly quoted, I have been unable to find hard evidence supporting its accuracy. In
my own experience, however, while dealing with Royal Air Force flight trainees
who apparently had been suffering from chronic, seemingly intractable, motion
sickness there have been those who did not appear to be able to adapt to provocative
motion and in a few of these cases, the individual did not seem to wish to do so.
Perhaps this has stemmed from the use of motion sickness as a means of escape
from an ill-considered choice of career. For all practical purposes, however, the
great majority of people are capable of adapting successfully to provocative motion.
© Springer Nature Switzerland AG 2019
T. G. Dobie, Motion Sickness, Springer Series on Naval Architecture,
Marine Engineering, Shipbuilding and Shipping 6,
https://doi.org/10.1007/978-3-319-97493-4_7
129
130
7 Adaptation to Provocative Motion
It is difficult to state how long people take to adapt to provocative motion. For
example, when people first go to sea, as a general rule, the majority will get their
sea legs within three or four days, but that will depend upon the sea state and
individual differences. In any group of men or women of the same age, there are
large differences in susceptibility to provocative motion, whatever the mode of
transport. One of the reasons is receptivity. This denotes the way in which an
individual processes the provocative stimulus within the central nervous system.
This suggests that a person with high receptivity transduces the sensory stimulus
more efficiently and that evokes a greater subjective experience than in one who has
low receptivity. As a sequence, therefore, it is suggested that the receptive person
would experience a greater sensory mismatch signal and suffer greater motion
sickness. A second factor is adaptability, or the rate at which a person adapts to an
atypical motion environment. Those who adapt slowly suffer from more severe
motion sickness and require longer adjusting to the motion than do the fast adaptors. This does not mean that slow adaptors are also receptive; the factors are
unrelated to all intents and purposes. There are also wide differences between
individuals in the way in which adaptation is retained between exposures to periods
of provocative motion. A person who demonstrates good retention of adaptation
remains free of motion sickness even if the exposures are sporadic. Those with poor
retention of adaptation are likely to suffer from motion sickness after relatively short
periods ashore between voyages, but would remain symptom-free if the shore time
was kept short. This demonstrates the significance of optimal scheduling and the
importance of retention wherein good habitability practices help to retain experienced crewmembers as long as possible.
7.1
Protective Adaptation
Reason and Brand (1975) have coined the phrase “protective adaptation” to
describe the observation that lengthy exposure to a particular type of provocative
stimulation generally causes a reduction, and eventual disappearance, of the
symptoms and signs of motion sickness in the majority of people. They have
stressed that this reduction has been entirely dependent on a complete lack of
change in the characteristics of the nature of the provocative stimulus. On that basis,
they have concluded that these changes lie within the organism and not the environment. When the conditions of sensory rearrangement have been qualitatively
unchanged over time, the motion responses have decayed. The duration of this
process has been found to be very variable, however, both in terms of the individual
and the surrounding circumstances. They have proposed that these protective gains
have been relatively rapid at first and have subsequently slowed.
Reason and Brand (1975) proposed three distinct stages in the sequence of
adaptive effects and after-effects. During the initial exposure to either inertial or
visual distortion, there has been a significant disruption of bodily movements and
psychomotor skills. They pointed out that motion sickness has manifested itself
7.1 Protective Adaptation
131
when maladaptation between the current spatial input and that expected, based on
previous experience, has been at its greatest. Second, as a result of continued
exposure over a sufficiently long time, the motion sickness responses have
diminished and might eventually disappear altogether. As an example of this protective adaptation, Hemingway (1946) studied 198 aviation students and found a
progressive decrease in the incidence of airsickness during the period of training.
He reported that 84% of students became airsick during the first few flights but that
number had dropped to 10.5% by the tenth flight. He also noted that this decrease
had not been linear. The decrease was more rapid during the first 5 flights in
comparison to the second 5 flights.
In similar vein, Joekes (1942) reported a reduction in the incidence of airsickness
over the first 10 h of training. In this case, it had only been 17% during the first few
hours of flying, whereas after 10 h, it had dropped to 0.5%. Clearly, the absolute
numbers were very different but the evidence of adaptation has been there. Joekes
also reported the occurrence of adaptation on swings. In a study involving 254 air
gunners he found that the incidence of swing sickness during the first session was
20%, but only 2.8% of those who had been sick failed to adapt during further
sessions of swinging. Manning (1943) also studied adaptation to swing sickness.
Dividing 100 unselected subjects into two groups, he had swung those in one of the
groups for 15 min every day for ten days, whereas those in the other group had only
been swung on the eleventh day. On that eleventh day, the incidence of sickness in
the first group that had been swung daily was only 18%, but in the other group it
was 42%.
Benson (1988) has pointed out that, in the long term, adaptation to provocative
motion is the best means of preventing motion sickness. He suggested that protective adaptation can best be obtained, and subsequently retained, by means of a
gradual introduction to the type of provocative motion to which the individual
would be exposed later. Having done so, he has recommended that this state be
maintained by means of regular and repeated practice in coping with that type of
stimulation. I would disagree that the stimulation has of necessity to be “similar” to
the individual’s specific environment and will discuss stimulus specificity/
generalization later in this chapter.
Adaptation to motion occurs, provided that there is sufficient time, such as
during prolonged sea voyages or lengthy periods in space, when an individual
becomes adapted to these new forms of environment. This brings us to Reason and
Brand’s third stage of adaptive effects, providing that the duration of exposure to a
provocative stimulus has been sufficiently long, the return to what had been the
previous natural circumstances has caused a return to motion disturbances. In this
situation, a motion sickness response can then occur when the adapted person
returns to his or her usual motion environment; this is known as mal de
debarquement.
132
7.2
7 Adaptation to Provocative Motion
Mal de Debarquement
Mal de debarquement, or “land sickness,” is a temporary feeling of unsteadiness
that includes sensations of tumbling, swinging, and disequilibrium, which some
passengers and crew members have reported when they have returned to land after a
long voyage. Although mal de debarquement has been mentioned in certain
important texts on the subject of seasickness (Reason and Brand 1975; Irwin 1881),
Gordon et al. (1992) were unable to find any studies specifically related to the
nature and extent of this response. They had carried out a computer search of the
literature which, at that time, had produced only one publication on the subject
(Brown and Baloh 1987), and that referred to persistent, not transient, mal de
debarquement. I shall return to the question of persistent mal de debarquement later
in this section.
Gordon and his colleagues then carried out a questionnaire study involving 234
fit crewmembers, aged between 18 and 38 years with no significant medical history,
from vessels in the range of 300–500 tonnes. The seagoing experience of these
participants has ranged from 1 to 150 months. The following information was
obtained:
(a) the frequency of mal de debarquement on a four point scale: (3 = very often;
2 = occasionally; 1 = only once; and zero = never);
(b) the latency of onset after disembarkation and duration of symptoms;
(c) other relevant factors: e.g., sea state and duration of voyage;
(d) present susceptibility to seasickness on an eight point scale, based on the
criteria described by Wiker et al. (1979);
(e) other motion sickness factors: e.g., recent incidence of nausea and vomiting in
heavy sea states and past history of seasickness.
These researchers found that a total of 171 crewmembers (73%) had experienced
mal de debarquement: of whom, 20 (9%) reported category 3 (very often); 86
(37%) category 2 (occasionally); and 65 (28%) category 1 (only once). In 127
persons (74%) the symptoms had appeared immediately and in 169 (99%) within
6 h. The duration of symptoms extended from a few minutes to 24 h, however, in
159 cases (93%) they lasted less than 6 h. They also found that this condition was
commonly associated with: extended voyages [115 crewmembers (67%)] and
heavy sea states [75 crewmembers (44%)].
These workers have opined that mal de debarquement was a common transient
and benign phenomenon that did not call for medical attention. Gordon and colleagues reported that the occurrence of land sickness was positively correlated with
all the characteristics of susceptibility to seasickness, but not with a person’s
experience at sea. That is to say, both experienced sailors and inexperienced passengers were liable to experience this post-voyage discomfort to a similar degree.
They also concluded that mal de debarquement could be explained within the terms
of the neural mismatch theory of motion sickness. When individuals have adapted
to the conflicting provocative stimuli at sea, they “get their sea legs.” On
7.2 Mal de Debarquement
133
disembarking from the ship, however, these sensorimotor patterns that they have
acquired at sea are no longer appropriate to the stationary environment. This can
cause “land sickness,” until such time as these individuals have readapted to the
new steady state, and got their “land legs” once more.
Gordon et al. (1995) have reported on a further questionnaire study designed to
provide a detailed description of the essential properties of this phenomenon and to
evaluate the relevance of prolonged habituation to the motion of the sea over
repeated voyages. This involved 116 fit male crewmembers, aged between 18 and
33 years, with no history of any kind of postural instability. These personnel were
drawn from ships in the class 300–500 tonnes, and they went to sea once or twice
per week on voyages that lasted between 5 and 8 h, over a period ranging from 1 to
120 months (average of 18 months). These workers evaluated the incidence and
clinical features of both mal de debarquement and seasickness in similar fashion to
the questions described in the previous study by Gordon et al. (1992). They judged
the effect of habituation by means of ascertaining whether or not the incidence of
this response changed according to the number of voyages; was the incidence
greater during their earlier or later voyages or has there been no difference?
Out of the total of 116 participants in the study, 83 (72%) reported having
experienced mal de debarquement, (15%—very often; 28%—occasionally, 29%—
only once, and 28%—not at all). The overall incidence was very similar to that
reported in the 1992 study (73%). However, the numbers in the first (very often)
category were (9%) and in the next (occasionally) category (37%) in that previous
study. The percentages in the other categories have remained essentially the same.
In terms of latency, the time of onset ranged from immediately on going ashore to
2 days. Eighty percent of the participants experienced this phenomenon within one
hour of disembarking and only 7 persons (6%) experienced latency greater than two
hours. In the previous study 74% of participants experienced this response immediately and all but 1% within 6 h. The duration lasted from 1 min to 2 days; in 88%
for less than six hours and only two persons reported responses greater than 24 h.
These results are similar to the previous 1992 study in which 99% reported a
maximum duration of 6 h. In terms of the duration of the voyage, 45% reported that
it usually occurred after a long voyage compared to 67% in the previous study.
Forty percent related these responses to rough seas, which is very similar to the
previous study (44%).
These workers concluded that indeed their results had confirmed the findings
reported by the previous team in 1992 and although this transient sensation of
unsteadiness had not required medical attention, there had been isolated instances,
particularly following exposure to rough seas, in which there was significant postural instability and impairment of driving ability. There seemed little doubt that
this apparently typical description of mal de debarquement was a transient and
relatively benign disturbance that occurred during the period of readaptation to a
land based environment, that had followed a period of exposure to a strong
provocative motion experience at sea.
Let us now turn to the question of persistent mal de debarquement. Brown and
Baloh (1987) have reported on six patients who had apparently suffered from
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persistent postural imbalance, ranging in duration from 2 months to 5 years following exposure to provocative motion. Five of the patients were female, ranging in
age from 38 to 71 years, and one was male aged 33 years. One of the female
patients had experienced this condition twice following boat trips and her most
recent experience had occurred after a 16-h flight that resulted in symptoms for
4 months. These patients did not apparently have significant histories related to
head trauma, headaches or drug abuse. Nor had they reported particular sensitivity
to provocative motion or significant motion sickness prior to the onset of this
particular phenomenon.
Brown and Baloh concluded that their patients could have been “experiencing a
persistent adaptation to a previous abnormal visual, vestibular or somatic environment, or some abnormality of the adaptive mechanism that has caused a failure
or delay of readaptation to the earth-stable environment.” The range of duration of
symptoms of four of the patients was 2–4 months, one was 10 months and the
oldest lady suffered for 5 years following a 70-day ocean voyage. These are certainly significantly longer than the more usual transient cases, suggesting that, as
these workers have suggested, this represented “a clearly definable group that may
be differentiated from the majority of dizzy patients…” It is interesting to note that
the majority (4 out of 6) of these patients were female and in the age range 38–
61 years, in the light of mounting evidence that age for age, females appear to be
more susceptible to motion sickness and this has been possibly attributed to hormonal disturbances.
Hain et al. (1999) have reported a patient survey involving 27 people with mal
de debarquement involving rocking and swaying of at least 1-month duration,
following a cruise or flight lasting for at least 4 h. They had also found that 26 out
of the total of 27 sufferers were middle-aged women (mean age 49.3 years). In this
study, the duration of the patients’ symptoms has been in the range from 6 months
to 10 years. Hain and his colleagues found that the symptoms of mal de debarquement did not respond well to either vestibular suppressants nor to physical
therapy, whereas Brown and Baloh had suggested that physical exercises that
involved walking and active head movements might speed up readaptation. The
issues concerning the use of vestibular training and cognitive-behavioural desensitisation training as they are related to motion sickness are discussed later in
Chaps. 9 and 12 respectively. I suspect that the addition of the cognitive component
to vestibular training would also speed up readaptation in cases of mal de debarquement, but have not yet had the opportunity to test this hypothesis.
7.3
Adaptation—Specific or General?
Although this question of adaptation is interesting of itself, from a practical
standpoint it is valuable to know if adaptation to one type of movement adapts an
individual to other forms of motion as produced by different “vehicles.” Gibson
et al. (1943) carried out a study using 150 student aircraft navigators involved in
7.3 Adaptation—Specific or General?
135
4000 swing sessions and 1250 flights. They found that regular daily amounts of
motion on a swing for 15 min each day over a period of two weeks before and
during the period of flying did not reduce the incidence of airsickness. Tyler and
Bard (1949) mentioned this question and although they acknowledged reports to the
contrary, they opined that the evidence available at that time supported specificity
of adaptation and a lack of transfer to other forms of motion; my work on
cognitive-behavioural training agreed with Gibson (see later in Chap. 12).
Reason and Graybiel (1970) have described a research programme in which they
investigated progressive adaptation to Coriolis accelerations aimed at designing an
adaptation schedule to protect against motion sickness induced in a rotating environment. They used 10 male subjects, aged 18–30 years, and provoked the subjects’ Coriolis accelerations by means of directed head and body movements in the
Pensacola Slow Rotation Room (SRR). When the training sessions had been
completed, the SRR was programmed in 1 rpm steps to a maximum velocity of
10 rpm. That was restricted to a lower level, however, if it had been deemed that
further increments would have led to acute motion sickness. At each velocity step,
the subject made the prescribed head and torso movements until one of three
outcomes occurred. First, the subject reached the “adaptation criterion” (see later),
in which case he proceeded to the next step following a 5-min rest with the head
fixed. If, however, the subject completed 45 sequences and had not yet reached that
criterion, he was given a 5-min rest with fixed head and then continued. Third, if the
subject reported the onset of motion sickness, he was immediately allowed to rest,
with fixed head, until these symptoms had gone and only then continued. The
arbitrary “adaptation criterion” that was used consisted of 3 completed sequences of
24 movements each, with negative response and apparent freedom from symptoms
of motion sickness. On reaching that criterion at the maximum velocity of 10 rpm,
the subject was given a 5-min rest period, after which the SRR was slowly brought
to a halt. The subject then made the same directed movements until having achieved
the adaptation criterion that constituted the end of the experiment.
Reason and Graybiel reported that the number of movements required to meet
the adaptation criterion has been systematically related to the absolute amount of
angular velocity. More such movements were necessary to obtain the same level of
adaptation as the speeds became higher, despite the fact that the step movements
were the same throughout. They also noted that 7 of the 10 subjects experienced
symptoms of motion sickness at various times during the experimental protocol and
in 4 of these subjects the symptoms had been sufficiently severe to cause early
termination of the experiment. Reason and Graybiel concluded that this indicated
that the occurrence of motion sickness had somehow interfered with what they
called the “normal process of adaptation.” This approach to providing protective
adaptation seemed to me to suffer from the serious disadvantage of overly provoking motion sickness responses. As you will see in Chap. 12, when I discuss the
rationale behind my motion sickness desensitisation training programme, I make
every effort to avoid provocative stimulation beyond an individual’s threshold of
response, so as to avoid reinforcing the concept of susceptibility to motion sickness.
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That will only serve to convince an individual that he or she really is exquisitely
sensitive to provocative motion and has little or no hope of adapting.
When referring to adaptive changes, Money (1970) has commented that these
were generally considered to have caused declines in response only in regard to the
specific stimulus that had been repeated. However, he also observed that examples
of stimulus generalisation, as distinct from specificity, have been reported in the
scientific literature. These apparently conflicting situations are not only interesting,
but they also have important implications in terms of dealing with motion sickness.
As Money has correctly stated, “Adaptation is one of the most effective therapies
for motion sickness.” But if the “specificity” theory were correct, that would create
significant difficulties in choosing the appropriate stimulus, or perhaps “stimuli” if
the person suffered from airsickness and seasickness. As I have noted earlier in this
chapter, Tyler and Bard (1949) were adamant that passive vestibular stimulation in
a rotating chair did not provide stimulation appropriate to a plane or ship. Despite
that, I have found that cross-coupled (Coriolis) stimulation, or even illusory motion
in an optokinetic drum can be used in a successful motion sickness desensitisation
programme. On the other hand, as we shall see in Chap. 13, behavioural desensitisation without cognitive intervention was not successful, which leaves us with the
question as to whether it is the cognitive component that permits stimuli to generalise. My colleagues and I have carried out the following experiments to address
this question. The results are by no means conclusive, but add further information to
this fascinating issue.
7.4
Reduction of Visually-Induced Motion Sickness
Elicited by Changes in Illumination Wavelength
Benson’s representation of a model of motion control and detection together with a
motion sickness response (Fig. 5.1 in Chap. 5) provides a useful diagram of Reason
and Brand’s sensory conflict hypothesis for the aetiology of motion sickness. As
you have seen in the last chapter, however, May and I (Dobie et al. 1989b) have
proposed an addition to Benson’s purely physiological concept of the aetiology of
motion sickness to take into consideration the personal attitudes, memories, and
past experiences (not just recent experiences) associated with motion environments
(Fig. 7.1). Briefly stated, this model assumes that some forms of provocative
motion lead to a sensory or perceptual disagreement, disorientation, and in turn,
heightened arousal and excitation. The degree of arousal is also likely to reflect
individual personality variables. Thus, the physiological reaction to this experience
and the parasympathetic rebound that may result constitutes what the sufferer
recognises as the symptoms of motion sickness. In addition, any anticipatory
arousal resulting from previous experiences with motion sickness can have a
synergistic effect on this response.
7.4 Reduction of Visually-Induced Motion Sickness Elicited …
137
Fig. 7.1 Theoretical stimulus generalization curves for classically conditioned responses to
conditioned stimuli of green and red (cs = conditioned stimulus)
It is possible that the anticipatory arousal stems from previous identification
between specific motion stimuli and the responses evoked by them. In that case, this
particular component of motion sickness might be conceptualised as a classical
conditioning of fear response. On that basis repeated exposures to a specific
stimulus that causes motion sickness should cause increased susceptibility to
motion sickness. Furthermore, such conditioning would be highly specific to the
particular characteristics of the stimulus. Conditioning with one stimulus and
testing with different stimuli would result in a reduction in the response proportional
to the difference. This relationship, that has been shown in Fig. 7.1, represents the
stimulus generalisation gradients found empirically in conditioning studies (Pavlov
1927). On the other hand, we already know that progressive increases in exposure
to motion stimuli can lead to decreases in susceptibility under controlled conditions.
In this experiment, my colleagues and I used a cross-adaptation design to test the
amount of generalisation of a motion stimulus (McBurney and Collings 1977). We
tried to ascertain whether the predicted associations formed by conditioning took
place between the motion stimulus and the perceptual disorientation, or between the
motion stimulus and the motion sickness response.
The experimental protocol included 16 young, healthy male U.S. Navy human
research volunteers, free of sensory or neurological problems, and either a negative
or mild history of motion sickness. Visually-induced apparent motion was produced
in the UNO optokinetic drum and gave rise to the illusory perception of
self-motion. The inner black and white striped surface of the drum was lit by two
150-W light sources located behind and beside the subject’s head, positioned so as
to avoid glare. Coloured acetate sheets (red or green) were positioned in front of
these lights to produce monochromatic illumination.
All subjects were exposed to 6 experimental sessions, each consisting of 5 trials.
Before and after each session, they completed a 21-question motion sickness
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symptomatology checklist. Magnitude estimates of the degree of illusory
self-vection and motion sickness, on a scale of 0–10, were made during the last 30 s
of each of the 4-min trials.
Other than switching the colour of the lights between sessions 3 and 4, all other
conditions across sessions and trials remained the same, including luminance and
temperature. In the first three sessions, half of the subjects experienced illusory
motion while the interior of the drum was illuminated in red light and the other half
of the subjects in green light. During the last three sessions the colours were
reversed. Thus, for one group, one colour has been associated with motion effects
during the first three sessions and the other colour has been substituted during the
last three sessions to test for the generalisation of motion effects.
The results have shown that the magnitude estimates of self-vection have
increased within sessions. This has indicated that the subjects perceived that they
have been rotating at a faster rate, with repeated illusory stimulation, despite the fact
that the drum was rotated at a constant 10 rpm throughout the study. Repeated
presentations of the motion stimulus caused an increase in perceptual disorientation,
within a session, that has dissipated between sessions and declined significantly
across the three-session blocks. Since the trends within the blocks were the same,
this suggested that adaptation generated under one colour has not transferred to the
other. This has indicated that adaptation of self-vection across sessions was quite
specific to the conditions that produced illusory self-motion.
The estimates of motion sickness increased within a session, and that might have
reflected the effects of increasing disorientation. However, this increase was slower
after the change in the colour of the interior illumination (Fig. 7.2). The increase in
the severity of motion sickness dissipated between sessions, and declined from the
first three-session block to the next. This has indicated that the subject’s adaptation
to motion sickness responses across sessions was not specific to the conditions of
illusory self-motion. Changing the interior illumination from one colour to the other
had not disrupted that adaptation.
The most interesting finding in this study was the change in the magnitude
estimates of motion sickness within a session before and after the colour change.
The increase in these estimates within a session was greater before colour change
than after. This seemed to indicate that adaptation was occurring but that it had not
been specific to the conditions that produced illusory self-motion. However, closer
inspection of the trials within sessions 3 and 4 showed an abrupt change that was
uncharacteristic of adaptation. One explanation for this effect could be associated
with stimulus generalisation. We have postulated that the motion sickness response
has become associated with the colour of the illusory stimulation during the first
three sessions, and that a reduction in that response has been elicited by the stimulus
when the colour has been changed.
This explanation is considered adequate for most of the data in Fig. 7.3, except
for the fact that significantly more motion sickness was reported on trial 1 after the
colour change than on trial 1 in the session before the colour had been changed.
This might have been due to a transient arousal evoked by the unfamiliar illusory
motion stimulation. This type of reaction has been discussed previously in relation
7.4 Reduction of Visually-Induced Motion Sickness Elicited …
Fig. 7.2 Mean magnitude
estimates of motion sickness
as a function of trials before
and after color change: all
sessions
Fig. 7.3 Mean magnitude
estimates of motion sickness
as a function of trials before
and after color change:
sessions 3 and 4
139
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to Lynn’s orientation reaction (1966), in Chap. 1. The results also indicated that the
adaptation of the motion sickness responses that was seen across sessions has not,
however, been specific to the conditions of the visual stimulation, since the colour
change has not disrupted this adaptation (Dobie et al. 1989a).
These findings would seem to have implications for the reduction of motion
sickness in applied settings. If, as we have seen, a simple change in the wavelength
of the environmental illumination results in a reduction in the rate at which motion
sickness develops, perhaps colour changes in other motion environments might also
increase tolerance to motion sickness in real world settings. On that basis, it is also
possible that other equally subtle and inexpensive manipulations might produce
similar reductions in subjective responses to provocative motion.
7.5
Generalisation of Tolerance to Motion Environments
As you will find at the beginning of Chap. 13, one of the questions that had been
raised when I first introduced the concept of managing seemingly intractable
motion sickness by means of cognitive-behavioural training had been the relevance
of cross-coupled (Coriolis) vestibular stimulation as a desensitising stimulus for
flight trainees. This had stemmed from concerns that Coriolis stimulation was not
sufficiently similar to motion in flight. That had raised a fundamental question
concerning the degree to which benefits gained in one situation would generalise to
another that was dissimilar. In the past, numerous observations have led to the
belief that adaptation to motion is quite specific to the particular type of motion
under which it has been acquired (Reason and Brand 1975; Benson 1988). Early
efforts to “inoculate” subjects using swings have not protected them against airsickness (Howlett 1957). Later, Homick (1979) reported that astronauts who had
adapted to the microgravity of space, nevertheless, still became severely seasick in
the recovery vessel.
I had used cross-coupled (Coriolis) stimulation quite successfully to help flight
trainees overcome their intractable airsickness as well as a sailor who had been
suffering from severe chronic seasickness (Dobie 1974). In the previous experiment
in this series, just described, subjects who had adapted under one monochromatic
light source generalised to the stimulus conditions involving a different
monochromatic light (Dobie et al. 1989a). Guedry (1965a) has reported that
adaptation to slow rotation in one direction resulted in suppression of responses to
rotational stimuli in both directions, when measured three weeks later. Graybiel
et al. (1965) reported that similar transfer of adaptation had occurred in two subjects
who had experienced walking on the walls of a slow rotation room and were later
asked to walk on the floor of the room.
Most theories concerning the aetiology of motion sickness have emphasised the
physiological reflexive responses to sensory mismatches and disorientation,
whereas my colleagues and I have argued that attitudes, memories, and past
experiences associated with motion environments are overlaid on these sequelae.
7.5 Generalisation of Tolerance to Motion Environments
141
Based on this view, management protocols that involved cognitive intervention
would be useful in facilitating adaptation to motion stimuli. Earlier in this chapter, I
have already alluded briefly to the results of a recent experiment which has
demonstrated that tolerance to provocative motion has been significantly increased
when subjects have received cognitive counselling in addition to adaptative training. On the other hand we have also shown in that study that adaptive training alone
is unsuccessful (Dobie et al. 1989b). This experiment is discussed in some detail in
Chap. 13. It may be that the reflexive (physiological) component has resulted in
specific adaptation to motion while the cognitive element has provided the generalisation of adaptation.
This investigation has, therefore, been aimed at examining the degree of generalisation of adaptation to motion that is obtained using different motion experiences during cognitively based counselling. If generalisation were achieved, it
would be expected that training on one device would result in increased tolerance to
other forms of provocative real or apparent motion.
Individuals whom we considered to have a significant history of motion sickness
were pre-tested in our optokinetic drum. I do not make that kind of decision
concerning the severity of motion sickness by allocating weighting factors to the
“so-called” severity of particular signs and symptoms, as some others have
described. Rather, I look at the overall pattern and severity of motion sickness as it
is related to the person’s exposure to potentially provocative motion devices. For
example I would consider that a “mild” history of motion sickness that has occurred
on every potentially provocative form of transport or device experienced by the
subject is more significant than a more severe response on one, or even a few, of
many devices experienced. Twenty of these selected individuals who had then
exhibited low tolerance to visually-induced apparent motion were assigned to 1 of 4
similarly matched groups. The subjects ranged in age from 19 to 48 years,
including 16 females. All of the subjects had normal or corrected visual acuity and
were apparently free of neurological and labyrinthine disorders.
Three types of apparatus were used to produce forms of real or apparent motion,
namely: the UNO optokinetic drum, which produced an illusion of circular vection
(self-motion); our rotating/tilting chair that produced passive cross-coupled
(Coriolis) vestibular stimulation and a standard video monitor that displayed a
white square that expanded in size from 1° to 9° of visual angle over repeated
periods of 800 ms. This stimulus had been chosen to produce a mild sensation of
linear self-motion. Subjects were pre-tested on all three devices during which
magnitude estimates of motion sickness, motion sickness symptomatology, and
tolerance scores were recorded. All pre-tests were limited to a pre-planned 20 min.
The subjects were then assigned to one of 4 groups. However, all of the groups
received 10 sessions of identical cognitive-behavioural counselling. Group 1
(Control) received no other training, while Groups 2, 3, and 4 received additional
training during sessions 2–10. Group 2 (Drum) was exposed repeatedly to the
rotating drum and Group 3 (Chair) to the rotating/tilting chair. Group 4 (Video) was
given experience with the expanding square stimulus on the monitor. Tolerance
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scores were very high for this type of stimulation and all subjects reached the
20-min limit quite early in training.
The main finding in the study provided some support for the concept that tolerance that has been gained on one device can transfer to another type of motion
experience (Dobie and May 1990). This was not universally true, however, and
appeared to have depended on the severity of the motion stimulus used during
training. The subjects in the chair group, who had experienced the most provocative
stimulus during training, exhibited significant increases in tolerance to
visually-induced apparent motion, as well as to actual rotary/tilting motion. Those
in the drum group exhibited significant increases in tolerance for visually-induced
motion, but did not exhibit significant increases in tolerance to rotary/tilting motion.
Neither the control group nor the video group exhibited significant increases in
tolerance to visually-induced motion or rotary/tilting motion. None of the groups
exhibited significant increases in tolerance to the least provocative stimulus (video)
owing to ceiling effects.
It is possible that transfer or generalisation of adaptation occurs more effectively
with vestibular stimulation. This has suggested that the most efficacious way to
produce generalised adaptation to motion environments should employ a very
provocative, perhaps vestibular, mode of stimulation. As always in my programmes, these stimuli did not exceed the individual’s threshold of response,
however. On the other hand, I strongly believe that a stimulus may be more
provocative to a given individual if it is unique to that person, in comparison to his
or her previous experience.
This feature has already been observed with regard to a US Navy pilot who
found illusory motion in the optokinetic drum much more provocative than
cross-coupled stimulation. In that case, I arranged to give a course of cognitivebehavioural training to that Naval aviator who suffered from severe seasickness that
significantly hampered his ability to enjoy sport fishing at sea. When that individual
was pre-tested in the rotating/tilting chair, there had been little or no motion
sickness response after 20 min exposure. In the optokinetic drum, however, he had
developed a motion sickness response very rapidly. The subject indicated that the
chair motion was similar to what he was used to in the air, but not so the sensation
of vection in the drum. I elected to use the vection stimulus in my course of
cognitive-behavioural training and that proved to be very effective. My client made
good progress during the training, demonstrating an ability to adapt to that form of
provocative motion. More important, however, he also volunteered to send me a
follow-up report some months later in which he affirmed that he no longer became
seasick even in the heaviest sea conditions. He also added the interesting fact that
he no longer even thought about becoming seasick. Perhaps this is an indication of
the importance of the cognitive input to stimulus generalisation that merits further
study. That unfamiliar characteristic of the stimulus may represent greater
“provocation” than merely increasing the quantum of a stimulus that is already
7.5 Generalisation of Tolerance to Motion Environments
143
familiar to that person. Previous results (Dobie et al. 1989b) have also suggested
that tolerance may be further enhanced by the addition of cognitive counselling.
These results have indicated that there are both specific and general components in
learning to tolerate motion environments.
7.6
The Transfer of Adaptation Between Actual
and Simulated Rotary Stimulation
It is clear that it is of great practical importance to have a good understanding of
adaptive mechanisms in both military and industrial applications. How well skilled
operators adjust to new and unique motion environments and how long they take to
do so are important questions. Must operators then readapt to non-motion environments? For example, we are already familiar with the problem of mal de
debarquement. Does repeated exposure to a specific motion environment provide
lasting benefits or not? These are important issues and there is only a limited
amount of experimental evidence available to address them.
Perceptual-motor experiments associated with a rearrangement of visual fields
have shown that considerable adaptation occurs, particularly if the experience is
active rather than passive. In addition, significant recovery is required in order to
readapt to the original unchanged spatial arrangements (Welch 1978). This raises
the central and critical issue. Can individuals adapt to provocative motion environments that are similar to those for which they are being trained or must the
training simulation be identical (Parker et al. 1987; Reason and Brand 1975)? In
other words, is adaptation general or specific? As we have already noted, Reason
and Brand have suggested that most research supports a specificity of adaptation, as
have Reason and Graybiel (1969b). However, as previously stated, there are significant exceptions to this concept (Guedry 1965b; Reason and Graybiel 1969a).
The current investigation has been designed to examine if motion sickness
counselling had significant effects on a subject’s responses in motion environments
that were not particularly severe. We also planned to extend the experimental
findings of Kennedy et al. (1987) and in particular to investigate this question of
specificity more closely. As in that study by Kennedy and his colleagues, we
questioned whether or not actual bodily rotation would transfer to conditions of
illusory motion. In that situation, the body is stationary, but an apparent sensation of
movement (vection) is produced in our optokinetic drum. We have also examined
whether adaptation to one direction of rotation would result in a reduced response to
that specific direction only, or if it would also generali se to the opposite direction
of rotation. The effects of adaptation were measured by comparing the differences
between pre- and post-test measures of dizziness, rotational velocity, and
heel-to-toe walking. We tested 17 females and 15 males, who were all healthy
volunteers from the University of New Orleans, aged between 18 and 30 years.
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They were then screened in our optokinetic drum to ascertain whether or not they
became disorientated with this type of stimulation.
The first means of stimulation (DRUM) was produced by the illusion of circular
vection in our optokinetic drum. Subjects were asked to indicate when vection
occurred and then to tilt their heads in the lateral plane, alternating 75° to the left
and right at a rate of 1 Hz, thereby inducing a pseudo-Coriolis response. The
second type of stimulation (SPIN) was that employed by Kennedy et al. The subject
was required to bend forward at the waist to an angle of 45° with one hand pointing
at the floor. The other arm was extended across the chest, under the pointing arm, to
grip the contralateral earlobe. This assured that the subject maintained a fairly stable
position during active bodily rotation. Each subject was then required to step,
circular fashion, around the point on the floor to which he or she was pointing. This
was continued until 10 revolutions were completed. Although the two modes of
stimulation were quite similar in terms of the speed of rotation (10 rpm), clearly
they differed in that one involved active bodily rotation and the other, passive
rotation of the visual field within the optokinetic drum. In addition, the drum
stimulation also involved pseudo-Coriolis stimulation through active head movements during exposure to the visual stimulation.
The subjects were pre- and post-tested on measures of disorientation after both
the active bodily rotation and the visually-induced illusory self-vection. Two groups
of 8 subjects received ten consecutive trials of active bodily rotation (SPIN)
(clockwise or counter-clockwise) for four consecutive days. The other 2 groups of 8
subjects followed the same protocol, except that they were exposed to that mode of
stimulation already described as DRUM.
The results showed that subjects who had been exposed to active bodily rotation
(SPIN) exhibited increased tolerance to visually-induced self-vection. On the other
hand, those exposed to visually-induced (illusory) self-vection (DRUM) did not
exhibit greater tolerance to actual bodily rotation. In addition, no support was found
for directional specificity. These results indicated that considerable adaptation to
disorientating rotary stimulation occurred despite the fact that dizziness was not
reduced during the exposure phase. However, this adaptation and the transfer of
adaptation from active rotation to visually-induced (illusory) stimulation seemed to
be general in nature and not tightly linked to the specific characteristics of the
motion involved (Dobie et al. 1990). This implies that the major benefit to be
gained from various types of visual simulation devices is in the field of operational
training procedures and any gains to be made in terms of adaptation may require
vestibular stimulation during training.
Clearly the jury is still out on this issue of stimulus generalisation. We seem to
have experimental evidence to support both specificity and generalisation. We also
have evidence that a cognitive component may play a significant part in allowing
generalisation to occur.
7.7 Summary
7.7
145
Summary
• Adaptation is a changing response to stimulus, the changing mechanism within
the body that is responsible for a response decline and, finally, the acquisition of
these changes.
• Visually-induced motion sickness seems to be reduced by changes in illumination wavelength. This may also have significance in terms of protection
afforded by other forms of environmental manipulation.
• It has been believed that adaptation to motion is specific to a particular type of
motion.
• Present studies, however, indicate that tolerance acquired using one device can
transfer to another motion experience and can be further enhanced with cognitive training.
• A major benefit of visual stimulation devices is in the area of operational
training procedures. Benefits for motion adaptation may require vestibular
stimulation.
• Further studies are required to answer this important question concerning
stimulus generalisation.
Reference
Benson AJ (1988) Motion sickness. In: Ernsting J, King P (eds) Aviation medicine, 2nd ed.
Butterworth-Heinemann Ltd., Oxford
Brown JJ, Baloh RW (1987) Persistent mal de debarquement syndrome: a motion-induced
subjective disorder of balance. Am J Otolaryngol 8:219–222
Dobie TG (1974) Airsickness in aircrew. AGARDOGRAPH No. 177, North Atlantic Treaty
Organization Advisory Group for Aerospace Research and Development, Neuilly-sur Seine,
France
Dobie TG, May JG (1990) The generalization of tolerance to motion environments. Aviat Space
Environ Med 61:707–711
Dobie TG, May JG, Fisher WD, Bologna NB (1989a) An evaluation of cognitive-behavioral
therapy for training resistance to visually-induced motion sickness. Aviat Space Environ Med
60:307–314
Dobie TG, May JG, Dunlap WP, Anderson ME (1989b) Reduction of visually-induced motion
sickness elicited by changes in illumination wavelength. Aviat Space Environ Med 60:749–754
Dobie TG, May JG, Guttierrez C, Heller S (1990) The transfer of adaptation between actual and
simulated rotary stimulation. Aviat Space Environ Med 60:1085–1091
Gibson WC, Manning GW, Kirkpatrick B (1943) Associate Committee on Aviation Medicine.
National Research Council, Canada. Report No. C2512. June 1943
Gordon CR, Spitzer O, Shupak A, Doweck H (1992) Survey of mal de debarquement. BMJ
304:544
Gordon CR, Spitzer O, Doweck I, Melamed Y, Shupak A (1995) Clinical features of mal de
debarquement: adaptation and habituation to sea conditions. J Vestib Res 5(5):363–369
Graybiel A, Kennedy RS, Knoblock EC, Guedry FE, Hertz W, McCleod M, Colehour JK,
Miller EF, Fregly A (1965) Effects of exposure to a rotating environment (10 rpm) on four
aviators for a period of twelve days. Aerosp Med 36:733–754
Guedry FE (1965a) Orientation of the rotation-axis relative to gravity: its influence on nystagmus
and the sensation of rotation. Acta Otolaryngol 60:30–45
146
7 Adaptation to Provocative Motion
Guedry FE Jr (1965b) Habituation to complex vestibular stimulation in man: transfer and retention
of effects from twelve days of rotation at 10 rpm. Percept Mot Skills 21:459–481
Hain TC, Hanna PA, Rheinberger MA (1999) Mal de debarquement. Arch Otolaryngol Head Neck
Surg 125:615–620
Hemingway A (1946) Selection of men for aeronautical training based on susceptibility to motion
sickness. J Aviat Med 17:153
Homick JL (1979) Space motion sickness. Acta Astronautica 1259–1272
Howlett JG (1957) Motion sickness. Can Med Assoc J 76:871–873
International Standard ISO 2631-1:1997(E) (7/15/1997) Mechanical vibration and shock—
evaluation of human exposure—part 1: general requirements. Irwin JA (1881) The pathology
of sea-sickness. Lancet ii:907–909
Joekes AM (1942) Correlation of swing sickness with airsickness. British Flying Personnel
Research Committee. Report No. 475
Kennedy RS, Berbaum KS, Williams MC, Brannan J, Welch RB (1987) Transfer of
perceptual-motor training and the space adaptation syndrome. Aviat Space Environ Med 58
(9, suppl):A29–A33
Lynn R (1966) Attention, arousal and the orientation reaction. Pergamon Press, Oxford
Manning GW (1943) Acclimatisation to swing sickness. Associate Committee on Aviation
Medical Research. National Research Council, Canada. Report No. C2623, Oct 1943
McBurney D, Collings V (1977) Introduction to sensation/perception. Prentice-Hall, Englewood
Cliffs, NJ
Money KE (1970) Motion sickness. Physiol Rev 50:1–38
Parker DE, Reschke MF, von Gierke HE, Lessard CS (1987) Effects of proposed preflight
adaptation training on eye movements, selfmotion perception, and motion sickness: a progress
report. Aviat Space Environ Med 58(9, suppl):A42–A49
Pavlov IP (1927) Conditioned reflexes: an investigation of the physiological activity of the cerebral
cortex. In: Andreo GV (trans, ed). Oxford University Press, London
Reason JT, Brand JJ (1975) Motion sickness. Academic Press, New York, NY
Reason JT, Graybiel A (1969a) Adaptation to Coriolis accelerations: its transfer to the opposite
direction of rotation as a function of intervening activity at zero velocity. NAMI-1086, NASA
Order R-93, Naval Aerospace Medical Institute, Pensacola, FL
Reason JT, Graybiel A (1969b) An attempt to measure the degree of adaptation produced by
differing amounts of Coriolis vestibular stimulation in a slow rotation room. NAMI-1084,
NASA Order R-93, Naval Aerospace Medical Institute, Pensacola, FL
Reason JT, Graybiel A (1970) Progressive adaptation to Coriolis accelerations associated with
1-rpm increments in the velocity of the slow rotating room. Aerosp Med 41(1):73–79
Tyler DB, Bard P (1949) Motion sickness. Physiol Rev 311–369
Welch RB (1978) Perceptual modification: adapting to altered sensory environments. Academic
Press, New York, NY
Wiker SF, Kennedy RS, McCauley ME, Pepper RL (1979) Reliability, validity and application of
an improved scale for assessment of motion sickness severity. USCG Technical Report
No. CG-D 29-79, U.S. Coast Guard Office of Research and Development, Washington, DC
Chapter 8
Prediction of Susceptibility to Motion
Sickness
Abstract It is very appealing to try to predict susceptibility to motion sickness.
Very many before me and no doubt many after, will pursue this goal. As you will
see, my experiences have been very disappointing. I spent many years evaluating
motion sickness history questionnaires and the seemingly predictive test of cupulometry—all to no avail. The more time I spend with people who suffer from
chronic motion sickness, the more intrigued I am by their stories. These stories
frequently seem illogical in terms of apparently widely different responses to
stimuli that seem to be very similar. Suffice to say that in our laboratory we are
frequently surprised by the responses of individuals. Those with a seemingly “bad”
history often do better on our motion devices than others whose history seems less
severe. We still have a lot to learn.
When I was assigned to HQ Flying Training Command, in the RAF, I started off by
using our Vampire aircraft to visit all the flying Training bases in the Command to
get a feel for how well the training was getting along and whether or not that there
were any problems that affected my job. It didn’t take long for me to discover that
airsickness was a really serious problem that was having an adverse effect on
training efficiency and causing the loss of valuable flight trainees. Although, as we
shall see later, this led me to introduce my cognitive-behavioural anti-motion
sickness training programme. In the meantime, my earlier attempts to deal with this
problem had centered around the concept of preventing airsickness by carefully
screening those candidates who wished to enter flight training. Apart from some
form of selection, the only other option at that time was to deal with the problem
when it arose, usually in the early days of primary flight training. In that case, it
meant using one of the available anti-motion sickness drugs and since they had
unacceptable side effects, this usage was limited to dual-only training sorties. That
was not a satisfactory solution from the instructor’s point of view because of the
need to medicate well ahead of take-off, which complicated flight planning.
© Springer Nature Switzerland AG 2019
T. G. Dobie, Motion Sickness, Springer Series on Naval Architecture,
Marine Engineering, Shipbuilding and Shipping 6,
https://doi.org/10.1007/978-3-319-97493-4_8
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148
8.1
8 Prediction of Susceptibility to Motion Sickness
Prevention of Motion Sickness by Candidate Selection
When confronted with this problem, I suppose that I raised the inevitable question,
“Can motion sickness be avoided altogether by carefully screening the new candidates for flight training, by checking their past histories?” Pre-selection always
seems an attractive solution, so at that early stage, I felt that it was well worth
trying. However, it is not only a difficult option to manage but, as it turns out, it also
carries serious penalties in terms of wasting potentially high quality applicants, as
we shall see later; for that matter provocative pre-testing was no better.
8.2
Selection by Means of Motion Sickness Questionnaires
In 1974, I had the opportunity to investigate the pre-selection approach in an
extensive study of questionnaires obtained from RAF flight trainees. Candidates’
histories of flight experience and motion sickness were obtained from 1000 randomly selected aircrew trainees before they began their basic flight training. These
motion sickness histories were collected in exactly the same format as that used at
the RAF Aircrew Selection Centre. The questionnaire data were then correlated
with the individual’s susceptibility to airsickness during basic flight training. That
information was entirely unsolicited, having been obtained from training reports
completed routinely after each sortie by flight instructors. These reports included
any reference to motion sickness and its effect on training performance.
In addition, I correlated the experimental questionnaire data with the subject’s
original data previously recorded when they were still civilian candidates at the
selection center. The objective of this approach was to assess the reliability of the
data recorded by the candidate regarding his history of motion sickness and flight
experience before being accepted for training, and to assess its value as a predictor
of airsickness during flight training. The results were as follows:
Previous Flight Experience: Although a positive correlation was found to exist
between prior flight experience and resistance to airsickness during flight training,
the exclusion of individuals without previous flying experience would not have
been cost-effective. Such a decision would have excluded only seven trainees who
became severely airsick during flight training and 22 candidates who did not. The
study also showed that despite considerable flying experience before entering the
RAF, 21 out of a total of 159 candidates became severely airsick during flight
training.
History of Motion Sickness: In a sample of 460 randomly selected pilot trainees, there was also a positive correlation between the incidence and severity of
airsickness during flying training and the individual’s pre-entry history of motion
sickness. However, if all candidates who had reported a history of severe motion
sickness were rejected, this would have eliminated 21 individuals who had subsequently become airsick, but that would have been at the expense of a further 38
trainees who did not.
8.2 Selection by Means of Motion Sickness Questionnaires
149
Candidates with no prior history of motion sickness were shown to be resistant
to airsickness during flight training. However, to have accepted only that group for
training would have entailed rejecting 281 candidates, which was more than 60% of
the total candidate population.
Turner and Griffin (1995) carried out an extensive study of various aspects of
motion sickness during a round-the-world yacht race, previously discussed in
Chaps. 2 and 4. In terms of the relationship of sailing experience prior to the race
and the occurrence of illness and vomiting, only those crewmembers classified as
“very experienced” have shown significantly lower incidences than any of the lesser
experienced groups. That group only represented 9% of the total number of
182 participants. This is another indication that previous history of motion sickness
per se does not constitute a practical selection tool.
Validity of Motion Sickness Questionnaires: Birren and Fisher (1947) carried
out a motion sickness history questionnaire study and evaluated the results by
means of the susceptibility to seasickness reported by those respondents in a survey
of the crew of a destroyer escort. All of them had spent a lot of time at sea and were
considered to have a good knowledge of their own susceptibility to seasickness, as
well as that of their shipmates. Each has been ranked in terms of susceptibility by
two independent observers including officer or petty officers who have had the
longest association with the particular individual being assessed. In all, 51 individuals made a total of 300 assessments concerning the susceptibility of others.
After these rating forms had been collected, we then collected the crewmember’s
own completely confidential motion sickness history questionnaire, that could not
affect his future in any way. These questionnaires included both the individual’s
previous history of motion sickness and his own personal evaluation of his susceptibility on a 5-point scale: (1) never get seasick, (2) rarely, (3) occasionally,
(4) often and (5) practically always gets seasick
Birren and Fisher found that individuals generally assessed their own susceptibility to motion sickness somewhat higher than the raters. In terms of the 10% of
crewmembers who were assessed as suffering from severe seasickness, there was
close agreement between the observers. They tested the reliability of the questionnaire by administering it during processing at boot camp in two ways. In one
group (n = 544), the individuals “have signed and answered the questionnaire
without being told that it was not part of the routine examining procedure.” In a
second group (n = 459), they had been told that “it was for research purposes only
and that no names have been required.” The researchers concluded that the scores
were not significantly different for the two groups.
Hardacre and Kennedy (1965) have also addressed the issue of identifying flight
students who were susceptible to motion sickness by means of motion sickness
history questionnaires, in an attempt to reduce flight training losses due to this
malady. In particular, they investigated the problem of obtaining truthful answers to
these questions. Three groups of 100 students arriving at flight school completed
their motion sickness questionnaires under three different conditions. One of the
groups has done so with the attached rider that their answers were strictly confidential for research purposes only, and would not affect their future careers
150
8 Prediction of Susceptibility to Motion Sickness
Table 8.1 History of motion sickness prior to entry into the RAF, recorded before and after
acceptance for flight training
Source of information
Sample
Affirmed
Percentage (%)
Medical form completed before entry
825
30
3.6
596 (16.2)a
59.6
Confidential questionnaire after entry
1000 (162)a
a
Number of candidates who admitted that their motion sickness had been particularly severe
in aviation. In the case of the second group, the same written rider was on the
questionnaire but it had been penciled out lightly, so that it was still readable, in
order to give negative assurance. For the third group, that rider had been omitted
altogether. There were no significant differences found among the answers to the
questionnaires across the three groups. Hardacre and Kennedy concluded that these
results suggested that incoming flight students answered the questionnaires in
equivalent manner regardless of any reassurances that had been made, or not.
I return to this important question because the incidence of previous history of
motion sickness recorded by applicants attending the RAF Aircrew Selection
Centre had seemed abnormally low for the type of population. In a random sample
of 825 candidates who underwent the initial selection procedure for flight training,
it was found that only 30 of them had admitted to any previous history of motion
sickness (3.6%). However, in a confidential questionnaire study carried out by
myself just before flight training began, (using an identical questionnaire) 596 out
of a total of 1000 aircrew trainees (approximately 60%) admitted that they had
indeed suffered from motion sickness prior to entry and 162 of them described it as
having been severe (Table 8.1). This coincided with the time when Hardacre and
Kennedy had carried out their study, namely on arrival at flight school. This larger
sample in my study included the majority of those 825 candidates who had originally claimed not to have experienced motion sickness when previously asked at
the Selection Center. This result has highlighted the difficulty of obtaining accurate
information on motion sickness histories before a selection decision has been made
as to whether or not to accept volunteers into the military for flight training. In the
case of the Hardacre and Kennedy study, however, the candidates had already been
selected for flight training prior to the questionnaire study, so that they could feel
secure in terms of acceptance at that stage, when completing the questionnaires.
8.3
Tests for Grading Susceptibility to Motion Sickness
Apart from the use of questionnaire data, volunteer student sailors and aviators have
commonly undergone various screening tests in an attempt to exclude those deemed
likely to become motion sick. Over the years, numerous provocative tests have been
used for this purpose (Reschke 1990; Lentz 1984; Miller and Graybiel 1970a, 1969;
Ambler and Guedry 1965). The first five tests, which are described here, have been
evaluated over many years at the Naval Aerospace Medical Research Laboratory
8.3 Tests for Grading Susceptibility to Motion Sickness
151
in Pensacola, Florida (Lentz 1984). The first two are cross-coupled (Coriolis)
angular acceleration stimulus tests. The next two are visual-vestibular conflict tests,
and the last of these five is an off-vertical test. This is followed by a report on tests
of vestibular function by Morton et al. (1947) and Bles et al. (1984).
Another, less provocative screening test that has been used in this context is
called cupulometry. This entails the measurement of the duration of the sensation of
turning, or the nystagmic response, evoked by a stopping stimulus. This test was
developed by van Egmond et al. (1948) in the Netherlands, and I later evaluated it
in depth (Dobie 1974, 1980, 1981). This particular test is discussed later in this
section. Finally, there is a short review of a reliability study of other provocative
motion tests carried out by Reschke (1990) for NASA and comments on the subject
of motion sickness predictors by others.
Brief Vestibular Disorientation Test (BVDT): This test involves passive
rotation of a subject at a constant rate of 90°/s (15-rpm) while seated erect with eyes
closed. After 30 s at that constant velocity, the subject makes 45° head movements
every 30 s in the following order: head right, upright, head left, upright, head right,
upright, head left, upright, head forward, upright. The total time of rotation is
5.5 min. At the end of the BVDT exposure, the subject completes a brief questionnaire concerning his or her reaction to the test. Observers rated the subject for
signs of motion sickness. Ambler and Guedry (1970) carried out a study to
determine if the brief vestibular disorientation test would be just as effective if
carried out at a rotational rate of 10-rpm, instead of the usual 15-rpm. This change
would reduce the disturbance caused to the subject. They concluded that this new
profile would provide a feasible alternative procedure, with results nearly comparable to those obtained at the higher rate of rotation. They were unable to compare
differences, however, in terms of predicting flight training failures because there
had been only 2 in the sample of 157 flight students. The BVDT test is considered
to be useful in detecting individuals who are extremely susceptible to provocative
motion, but less useful for those of average susceptibility. In-flight airsickness has
not correlated highly with these test scores (Lentz 1984).
Coriolis Sickness Susceptibility Index (CSSI): In the CSSI test, a seated
subject is required to make 90° head movements toward the four quadrants in the
following order: front, upright, pause; right, upright, pause; back, upright, pause;
left, upright, pause; front, upright, rest. The velocity of the chair is chosen on the
basis of several preliminary tests and questionnaires, and is limited to one of the
following constant velocities: 2.5, 5, 7.5, 10, 12.5, 15, 20, 25, or 30 revolutions per
minute (rpm). The test usually lasts less than 15 min.
The CSSI scores are calculated by multiplying the number of head movements
by a factor “E.” This factor is the average relative stimulus effect of a single head
movement. Miller and Graybiel (1970b) have found that this “E” factor could be
expressed as a linear function (log/log) of chair velocity. The distribution of scores
obtained on the CSSI test has suggested that it would be best suited for detecting
subjects who were relatively resistant to motion sickness (Lentz 1984).
Visual-Vestibular Interaction Test (VVIT): In this test a subject, seated erect
in a closed chamber, is passively oscillated sinusoidally at 0.02 Hz, with a peak
152
8 Prediction of Susceptibility to Motion Sickness
angular velocity of ±155°/s. The axis of rotation is vertical. The chamber in which
the subject is seated remains dark until a test data display is illuminated. The subject
is then required to retrieve data from that display by using the coordinate system to
find the corresponding number embedded within the test matrix. Lentz (1984) has
observed that the complexity of the display used in this test plays an important part
in defining its nauseogenic quality. However, this test has shown a generally low
correlation with airsickness reported in flight.
The Sudden-Stop Vestibulo-Visual Test (SSV): In this test, a subject is
accelerated at 15°/s/s to a constant velocity of 300°/s, holding that velocity for 30 s
before decelerating rapidly to a stop, in 1.5 s, followed by a 30-second rest. This
sequence is repeated 20 times with the subject’s eyes blindfolded, followed by
another 20 times with the eyes open. If necessary, this manoeuvre is repeated an
additional 20 times with eyes open, but with rotation in the opposite direction.
In the eyes-open condition, the subject is surrounded by a dark cylindrical surface
on which there are six narrow, vertical white stripes, evenly spaced. The subject
views this surface until reaching the “slight nausea” endpoint, as defined by
Graybiel et al. (1968), see Table 6.1 in Chap. 6. On reaching this point, the subject
receives a score calculated from half the number of stops with eyes covered, plus
the number of stops with eyes open, plus twice the number of stops after the
direction of rotation has been reversed. This test has been more recently evolved
than the previous tests and was still under evaluation.
Tilted Axis Rotation Test (TART): In this test, unlike the previous one, the
subject stands erect securely fastened in a litter device, rotated about an axis that
can be tilted relative to gravity. The subject is blindfolded and the test is carried out
in a darkened room. In the first trial, the subject is accelerated clockwise at 25°/s/s
to a constant velocity of 60°/s, with the axis of rotation vertical. This velocity is
maintained for 90 s; the subject is then decelerated to a stop at 25°/s/s. The next
trial is identical, except that it is rotated counterclockwise. In the third and fourth
trials, the axis of rotation is tilted 30° off the vertical and the tests are repeated in
that axis, using the same protocols as described for the first and second trials. The
subject is always stopped in the nose-up position. In the fifth and sixth trials, the
subject remains tilted at 30° off the vertical and is again accelerated at 25°/s/s.
During these trials, however, a constant velocity of 120°/s is used. The interval
between trials is approximately five minutes.
The subject completes a brief questionnaire after the test concerning his or her
reaction to the test. In addition, observers rate the subject for signs of motion
sickness. The rating system is the same as that used after the BVDT and VVIT tests.
Because subjects commonly abort before completing the TART test, the self-rating
and tester scores are weighted, somewhat arbitrarily, according to the number of
trials completed. If all six trials are completed, the scores are multiplied by 0.65,
based on evidence that approximately 65% of a random unselected group of subjects complete that number. For similar reasons, the scores of subjects who complete fewer trials have been calculated as follows: after five trials, the scores are
multiplied by 0.73; four trials, by 0.90; and three trials, by 0.98. Subjects who do
not complete the third trial are assigned their raw scores.
8.3 Tests for Grading Susceptibility to Motion Sickness
153
Lentz (1984) has opined that all of these tests have a fairly low correlation with
conditions in the real world. He has suggested that for mass testing of subjects one
would have to consider reducing the false positive predictions and that an even
milder test might better identify the extremely motion sick individuals. These
provocative tests have, however, met with varying degrees of success and should
not be neglected completely.
Vestibular Examination: Morton et al. (1947) reported a study in which
31 subjects were given a caloric test using 3 cc of ice water and both the time of
onset of nystagmus and past pointing were recorded, together with the subject’s
degree of discomfort. Twenty-five of these subjects were then tested on their
“Roll-Pitch Rocker” previously described in Chap. 4, but no correlation has been
found between their vestibular responses and susceptibility to motion sickness.
Bles et al. (1984) have also investigated several tests in an attempt to find
parameters that would predict susceptibility to airsickness. In that study, they used
two sub-groups: One consisted of 39 naval subjects (male only) who were susceptible to seasickness; the other of 20 non-naval controls (14 males and six
females) who had participated in an expedition without showing signs of chronic
seasickness. Routine visual and otological examinations, including caloric irrigation, have been carried out on all subjects. No abnormalities were found during
routine examination of the control group. However, things were different in the case
of the subjects who were susceptible to seasickness. Two subjects have shown
evidence of cervical pathology. One showed a slight impairment of smooth pursuit
and fixation suppression, and once, during caloric irrigation, a congenital nystagmus was observed with significant asymmetry. In two other subjects, caloric irrigation was interrupted because of severe vomiting and in one case could not be
performed because of a perforated eardrum. In the group of 36 subjects susceptible
to seasickness, a significant labyrinthine predominance (>30%) was observed five
times.
All of the 20 control subjects and 38 of those subjects susceptible to seasickness
have been examined in the tilting room at TNO. The amplitudes of the induced
lateral body sway were greatest for the motion sickness susceptible subjects, particularly at a frequency of 0.2 Hz.
Bles et al. were unable to identify a sufficiently accurate parameter to predict
susceptibility to chronic seasickness. They did, however, discover that routine
vestibular examination has revealed a high percentage of abnormal values. Their
findings in the tilting room suggested that subjects who were susceptible to seasickness were much more visually oriented than the controls, although a clear
overlap existed. As a result, they concluded that a vestibular imbalance might
enhance susceptibility to motion sickness. Interactions of the otolithic and visual
systems might be organised differently in those who were susceptible to
seasickness.
Cupulometry: I chose cupulometry as a potential selection test in preference to
the more provocative tests because it had the advantage that the vestibular stimulus
was mild and didn’t induce motion sickness. This technique was developed by van
Egmond et al. (1948) as a way to examine the cupula-endolymph system of the
154
8 Prediction of Susceptibility to Motion Sickness
inner ear quantitatively. Hulk and Jongkees showed the normal cupulogram in the
same year (1948). Cupulometry is a turning test that measures the duration of the
post-rotatory after-sensation evoked by a stopping stimulus. Brown (1874) noted
that the sense of rotation, like others, is subject to the illusion of rotation when there
is none. During angular rotation at a constant rate, the sensation of rotation gradually diminishes and stops altogether. If the stop is sudden, the subject experiences
the sensation of rotation in the same axis, but opposite direction. The duration of
this after-sensation supplies the raw data for plotting a cupulogram.
In my study, the subject was seated in a blacked-out, soundproof box mounted
on a platform that could be rotated in either direction. By using a number of
turntable velocities, the duration of the after-effects produced by various angular
(stopping) impulses were recorded and the appropriate stimulus-response graph, or
cupulogram, was plotted (Fig. 8.1). The gradient of this straight-line relationship
(slope) was considered by van Egmond et al. (1948) to be a measure of the time
constant of the exponential decay of the after-sensation and hence of cupular
restoration following deflection by the angular velocity step. Extrapolation of the
cupular slope line to intercept the abscissa gives a measure of the impulse intensity
at threshold.
De Wit (1953) used cupulometry as a way of identifying groups of subjects with
markedly different levels of susceptibility to seasickness and compared their results
with those of a control group. His results showed that the mean slope of the
cupulogram for the control group was 9 s; for the motion-resistant group, 4 s; and
for the motion susceptible group, 13 s.
Fig. 8.1 Schematic cupulogram
8.3 Tests for Grading Susceptibility to Motion Sickness
155
The originators of the test stressed the advantages of cupulometry over the
classical Bárány (1908) turning test, as have others (van Egmond et al.; De Wit
1953; Aschan et al. 1952). The main reasons were twofold. First, in the Bárány test
the duration of cupular deflection exceeded “physiological limits.” Second, and
more important still, the effect of the acceleration stimulus had not worn off before
the deceleration impulse took place (Aschan 1954). These difficulties have been
overcome by the design of the technique of cupulometry.
The characteristics of the mean cupulogram that I obtained in a pilot study were
of the same order as those obtained by previous workers (Dobie 1965). However,
there were apparent discrepancies in the relationships between the slope and
threshold values and the susceptibility to airsickness. Contrary to the data published
by the previous workers, the non-airsick group had a steeper mean slope value. In
view of the relatively small sample, however, I decided to continue the investigation and as a result, 1000 subjects have been tested in all.
The mean slopes and thresholds of the yaw axis sensation cupulograms of the
1000 subjects in the series (including the 158 subjects in the pilot study) were 7.7 s
and 2.4°/s as seen in Table 8.2. The test population was then broken down into
sub-groups according to previous flight experience, history of motion sickness, and
subsequent susceptibility to motion sickness during flying training. Subjects were
divided into five groups according to the amount and type of flying experience prior
to undergoing cupulometry. The first three groups are self-evident, but the
remainder requires further explanation.
The subjects in group PFE UAS each had some 200 h flight experience,
including solo flying, in light aircraft at University Air Squadrons. They differed
from those in group PFE 2 not only in the amount of flying; they were in regular
flying practice and had a a higher academic background. The mean cupulogram
characteristics for these five groups are shown in Table 8.3. There is no significant
correlation between the mean values for slope and threshold and flight experience.
The subject population was then divided into three groups according to the
severity of their motion sickness, prior to the cupulometric test, see Table 8.4; there
was no significant correlation between the mean values for slope and threshold of
the cupulograms and the subjects’ prior history of motion sickness.
Finally, the cupulogram characteristics were examined as predictors of motion
sickness susceptibility during subsequent flight training. The unsolicited data
concerning student airsickness during training were obtained at the end of basic
flight training, directly from instructors’ existing post-flight reports for the whole
training. This has consisted of some 180 flight-hours in single-engine jet trainers.
Due to training wastage and some non-availability of documents caused by
Table 8.2 Summary of population mean slope and threshold values of yaw axis sensation
cupulograms (1000 subjects)
Mean slope and Threshold Values
Population Mean Slope
Population Mean Threshold
7.7 s
2.4° s−1
156
8 Prediction of Susceptibility to Motion Sickness
Table 8.3 Mean slope and threshold values of yaw axis sensation cupulograms related to
previous flying experience (PFE)
Type of subject
Number of subjects
Slope (s)
Threshold (° s−1)
All Types
1000
7.7
2.4
PFE 0
110
7.7
2.4
PFE 1
438
7.7
2.4
PFE 2
318
7.8
2.3
PFE UAS
81
7.7
2.5
PFE X
53
7.8
3.0
PFE 0 = No previous flight experience
PFE 1 = Leas than 10 h flying or passenger only
PFE 2 = 10–100 h fiight time
PFE UAS = Ex-university air squadron student pilots PFE X = Graduate flight crew
Table 8.4 Mean slope and threshold values of yaw axis sensation cupulograms related to
previous history of motion sickness (PHMS)
Type of subject
Number of subjects
Slope (s)
All Types
1000
7.7
PHMS 0
404
7.5
PHMS 1
434
7.9
PHMS 2
162
8.0
PHMS 0 = No previous history of motion sickness
PHMS 1 = Previous history of mild motion sickness
PHMS 2 = Previous history of severe motion sickness
Threshold (° s−1)
2.4
2.5
2.4
2.3
administrative problems entirely unrelated to this investigation, the population
sample had been reduced to a total of 485 out of the original 1000 students who
underwent cupulometry. The population was divided into three groups according to
the degree of performance decrement caused by airsickness. The mean cupulogram
characteristics for these three groups are shown in Table 8.5.
There is no significant correlation between the mean values for slope and
threshold and the subjects’ susceptibility to airsickness during subsequent flight
training. The original workers suggested that subjects who were susceptible to
motion sickness produced cupulograms with the steepest slopes. That has not been
confirmed in the main study. Finally, I decided to examine two groups of subjects
who had been widely different in terms of their susceptibility to motion sickness
and flying experience. These groups consisted of trainee pilots who had experienced severe airsickness during their flight training (SHAS 2) and the other group
consisted of flight instructors who were in current acrobatic flight practice and who
had never suffered from airsickness of any kind (PFEX). The cupulograms of these
two highly separate groups are shown in Table 8.6. It is quite evident that there is
no correlation between the mean values for their slope and threshold and their
susceptibility to motion sickness.
8.3 Tests for Grading Susceptibility to Motion Sickness
157
Table 8.5 Mean slope and threshold values of yaw axis sensation cupulograms related to
subsequent susceptibility of airsickness during flight training (SHAS)
Type of subject
Number of subjects
All Types
485
SHAS 0
266
SHAS 1
120
SHAS 2
99
SHAS 0 = No recorded evidence of airsickness
SHAS 1 = Evidence of mild airsickness
SHAS 2 = Evidence of incapacity due to airsickness
Slope (s)
Threshold (° s−1)
7.7
7.8
7.7
7.4
2.4
2.4
2.3
2.3
Table 8.6 Comparison of slope and threshold values of yaw axis sensation cupulograms for
group SHAS 2 (intractably airsick) and group PFE X (airsick resistant)
Type of subject
Number of
subjects
Slope
(s)
Threshold
(° s−1)
Severe Airsickness during Training (SIIAS
2)
Experienced Flight Instructors (PFE X)
99
7.4
2.3
53
7.8
3.0
The mean slope and threshold values from my main study and pilot study are
shown in Table 8.7, together with the results already published by others at that
time. In view of the range of values, the mean results are seen to be comparable.
The original workers, van Egmond et al. (1948), have described a linear relationship between a log plot of the impulse against a linear plot of the duration of
post-rotatory after-sensation. In my series, however, a considerable number of the
cupulogram slopes were found to be nonlinear. This is not associated with a wide
dispersion of the individual points. Linear, as opposed to curvilinear, cupulograms
had been produced by 651 of the 1000 subjects. The criteria of linearity were that
the regression had to be significant for the slope values measured in forward or
reverse directions, or both, and if the correlation coefficient was less than 0.7 on
either slope, both were discarded.
When the 349 curvilinear cupulograms were discarded and the mean slope and
threshold values were recalculated, there was little difference in the mean values.
The exclusion of nonlinear cupulograms has still failed to establish a significant
difference between the mean slope and threshold values in relation to the various
subgroups in the subject population according to previous flying experience, previous history of motion sickness, or subsequent susceptibility to airsickness during
flight training. Thus, even if only linear regression cupulograms were used,
cupulometry failed to discriminate between groups of subjects with widely differing
flight experience or susceptibility to airsickness.
The cupulograms were then reviewed further in an attempt to identify other
features that might provide the key to this apparent discrepancy between the present
series and that of the original workers in terms of using cupulometry as a selection
tool. Apart from nonlinearity, it was apparent that certain cupulograms showed
158
8 Prediction of Susceptibility to Motion Sickness
Table 8.7 Summary of results from yaw axis sensation cupulogram studies by various authors
Sources of published
results
Number of
subjects
Mean slope
(s)
Mean Threshold
(° s−1)
Hulk and Jongkees (1948)
Aschan ct al. (1952)
De Wit (1953)
Aschan (1954)
Benson et al. (1966)
Benson (1968)
Dobie (1980)
Dobie (1981)
50
320
22
100
14
142
158
1000
7
8.2
9.0
8.0
7.8
6.8
7.2
7.7
2.5
4.6
3.0
Not reported
0.7
1.4
1.4
2.4
widely differing characteristics. However, in a number of cases where the slope
values of the cupulograms were of the same order, there was a marked difference in
the extrapolated threshold value. Since nearly a third of the cupulograms were
nonlinear, I questioned the validity of extrapolation to threshold. I decided, therefore, to summate the recorded post-rotatory after-sensation times (designated “total
after-sensation time”) and relate these to the characteristics of the various
sub-groups previously described.
The second feature that came to light from this study of the characteristics of the
cupulograms had already been mentioned by the original workers; namely, that
some subjects showed marked directional preponderance. De Wit (1953) had made
the point that directional preponderance might indicate some pathological damage
to the inner ear and referred to this group of subjects as the so-called “unspecific
seasick.” In the present population, however, it was unlikely that any of the subjects
had suffered otological damage since all were medically fit flight trainees, who had
recently undergone their ‘Ear Nose and Throat’ medical screening. It was an
important point, however, because, as we have already learned, Bles et al. (1984)
found that routine vestibular examination has noted the existence of vestibular
imbalance as a possible contributor to the etiology of motion sickness. Figure 8.2
shows a diagram of a curvilinear cupulogram on which a mean slope has been
drawn, extrapolated to threshold; being questionable, I decided to measure “total
after-sensation time” in all cases; namely the summation of the recorded
post-rotatory after-sensation times in both directions. Directional preponderance
refers to the difference between the cupulogram characteristics related to the
direction of rotation of the turntable. This is shown diagrammatically in Fig. 8.3. In
practice, the curves were not always so clearly separated and directional preponderance was measured by subtracting the total after-sensation time in one direction
from that in the other direction. The subtraction of the lesser from the greater in all
cases is represented by the solid lines between the upper and lower points in
Fig. 8.3. This was chosen because it was difficult assess the significance of adaptation according to whether the subject experienced a clockwise (forward) rotation
before the counterclockwise (reversed) rotation, or vice versa. It has already been
8.3 Tests for Grading Susceptibility to Motion Sickness
159
Fig. 8.2 Diagram showing a curvilinear cupulogram
Fig. 8.3 Diagram of a cupulogram showing directional preponderance
pointed out that the direction of the first run at each speed was randomised across
subjects.
The results of these assessments are shown in Table 8.8. There is no significant
difference (chi-squared test) between the total after-sensation times, or the directional preponderance of the various groups, irrespective of their (A) flying experience, (B) history of motion sickness, or (C) susceptibility to airsickness during
flight training. The mean values are remarkable in their similarity when compared
160
8 Prediction of Susceptibility to Motion Sickness
Table 8.8 Yaw axis sensation cupulograms: total after-sensation time and directional preponderance related to (a) previous flying experience (PFE), (b) prior history of motion sickness
(PHMS), and (c) susceptibility to airsickness during flight training (SHAS)
Group
codes
After-sensation times (s)
Mean
values
(a) PFE
(b)
PHMS
(c)
SHAS
0
1
2
UAS
X
Total
0
1
2
Total
0
1
2
Total
195.4
189.2
204.1
182.6
174.1
193.3
184.4
193.9
213.8
193.3
189.7
190.0
201.3
192.0
Range
27.9–488.5
22.5–546.6
27.9–748.8
41.7–661.1
22.0–425.6
22.0–748.8
22.5–546.6
22.0–579.7
41.7–748.8
22.0–748.8
22.5–661.1
41.7–534.3
46.9–562.7
22.5–661.1
Directional
preponderance(s)
Mean
Range
values
Number of
values
12.9
11.6
12.1
11.4
13.1
12.0
11.4
12.4
12.4
12.0
12.0
10.0
10.9
11.3
108
431
312
80
53
984
397
428
159
984
267
117
92
476
0–73.4
0–66.9
0.1–82.3
0.1–43.3
0.2–82.2
0–82.3
0.1–79.0
0.1–82.3
0.1–61.1
0–82.3
0.1–82.3
0.2–34.4
0.1–53.9
0.1–82.3
with the total range of values that they represent. These particular characteristics
of the cupulogram are no more useful than the slope and threshold values as a
means of identifying the various groups of candidates examined.
At a later date, Bles et al. (1984), in the Netherlands, obtained complete cupulograms from a group of 21 naval subjects who had been susceptible to seasickness.
They had also found, as I had, that there was no difference in the slope of the
cupulograms for seasick individuals and controls. In view of the failure of cupulometry to discriminate between groups of widely differing experience, I am of the
opinion that the evoked vestibular responses have a similar distribution in all
subjects who are otologically fit. The major differences between cupulograms
seemed to be an expression of the manner in which different individuals assessed
and reported their post-rotatory after-sensations. These are not necessarily independent of end-organ responses or the level of adaptation within the vestibular
sensory system. No consistent relationship to the state of habituation to motion
(expressed as a reduced susceptibility to airsickness) has been found to exist,
however. I concluded that cupulometry could not be used as a selection tool to
identify susceptibility to motion sickness in the air, and probably not in any other
form of this malady either.
8.4 Comments Regarding Prediction
8.4
161
Comments Regarding Prediction
Hutchins and Kennedy (1965) have investigated whether or not flight student scores
on the Pensacola motion sickness questionnaire (MSQ) would supplement their
multiple prediction formulae regarding either successful completion of flight
training or voluntary withdrawal from training in a population of 802 flight students. They found that the MSQ scores have indeed been significantly related to
both of these criteria. They also reported that the addition of the MSQ scores to
their multiple prediction formulae has significantly improved the multiple validity
for predicting these outcomes; namely: success or voluntary withdrawal from
training. One must stress again that these questionnaires were completed after the
individuals had already been accepted and entered into the training programme.
Reschke (1990) has investigated the test reliability of the Coriolis Sickness
Susceptibility Index (CSSI) test, the Staircase Velocity Motion Test (SVMT) and
the KC-135 Parabolic Flight Static Chair Test (KC-135 PSCT). The CSSI test has
already been described. The SVMT is a modification of that test, in which the
cross-coupled (Coriolis) angular acceleration progresses from low-level to maximum stress stimulation, rather than staying at a single fixed constant velocity.
The KC-135 PSCT is a provocative test of motion sickness susceptibility during
parabolic flight by means of a tally of the subjects’ symptoms of motion sickness
through the duration of these maneuvers. There are approximately 40 parabolas per
flight, each consisting of 24 s of weightlessness and 30–60 s of a 2-G pull-up.
Reschke reported that all of these tests have stable, reasonable reliability. He has
pointed out, however, that it has to be demonstrated that the measure of space
motion sickness is well enough assessed so as to be forecast by any predictors. He
concluded that none of the individual tests would be an adequate predictor but has
suggested that all of these, taken together with other variables, might provide a
predictive index.
Kennedy et al. (1990) have published a comprehensive review of motion sickness predictors. They concluded that most of the best of those available were still
capable of some improvement. In their opinion, that approach seemed to be more
fruitful than seeking new predictors of adaptability and transfer of adaptation, with
the possible exception of plasticity. They have classified current predictors, from
best to worse, as follows: operational measures; provocative tests; motion sickness
history; personality and perceptual style; physiological measures of autonomic and
sensory function. Since operational measures may not always be available, they
have recommended that a composite of the motion sickness history questionnaire,
physiological variables, and standardised laboratory provocative tests might serve
as the best predictor set.
The further complication remains, however, that many who perform badly on
such tests can be trained to overcome motion sickness. In addition, evidence supports the notion that, in the long run, many of these people turn out to be above
average in many ways. This assessment has been based on the results that I found
pertaining to the military personnel in my cognitive-behavioural training
162
8 Prediction of Susceptibility to Motion Sickness
programme. For example, those trainees have been rated highly in their flying
ability after overcoming their motion sickness (Dobie 1974). As Money (1970) has
pointed out, and in keeping with the previously noted observations of Collins and
Lentz (1977), most measures of susceptibility to motion sickness would probably
have eliminated Julius Caesar, Admiral Lord Nelson and Lawrence of Arabia, all of
whom were unusually susceptible to this condition.
Since the various forms of screening that have been investigated had all been
found to be unproductive and the problem of airsickness among flight trainees
continued, I dropped the idea of using selection as a means of overcoming the
problem. This left me with no option but to turn my attention to ways of either
preventing or managing the malady by some form of training. These approaches
will be discussed in the following chapters, together with my reasons for adopting
my cognitive-behavioural training approach for the management of chronic motion
sickness.
8.5
Summary
• Pre-selection has been viewed as a possible solution to the problem of screening
for flight training candidates who might be susceptible to motion sickness.
• The Motion Sickness Questionnaire has been used to obtain information on a
subject’s previous flight experience and history of motion sickness. A problem
with the Motion Sickness Questionnaire is the difficulty of obtaining accurate
information on motion sickness histories, particularly at the time of
decision-making in terms of acceptance into the military.
• Even if accurate history information could be obtained, however, previous
history of motion sickness per se did not constitute a practical selection tool.
• Apart from the use of a questionnaire, numerous provocative screening tests
have been used. These include: Brief Vestibular Disorientation Test, Coriolis
Sickness Susceptibility Index, Visual-Vestibular Interaction Test, Sudden-stop
Vestibulo-Visual Test, Tilted Axis Rotation Test and Cupulometry.
• Cupulometry cannot be used as a selection tool to identify susceptibility to
motion sickness, based on the failure to find a significant correlation between
rhe mean values for slope and threshold and susceptibility to motion sickness
and further validation of other tests is still required.
• Apart from these selection limitations, the fact that those who were returned to
flying following their course of cognitive-behavioural desensitisation have done
so well both in training and subsequently on their squadrons, has also suggested
that selection might not be the best solution.
References
163
References
Ambler RK, Guedry FE (1965) The validity of a brief vestibular disorientation test in screening
pilot trainees. NAMI-947, Joint Report US NAMI & NASA, Naval Aerospace Medical
Institute, Pensacola, FL
Ambler RK, Guedry FE (1970) Reliability and validity of the brief vestibular disorientation test
compared under 10-RPM and 15-RPM conditions. NAMRL-115, US Naval Aeromedical
Research Laboratory, Pensacola, FL
Aschan G (1954) Response to rotatory stimuli in fighter pilots. Acta Otolaryngologica
116(suppl):24–31
Aschan G, Nylen CO, Stahle J, Wersall R (1952) The rotation test: cupulometric data from
320 normals. Acta Otolaryngol 42:451–459
Bárány R (1908) Die modernen untersuchungsmethoden des vestibularapparates und ihre
praktische bedeutung. Med Klin 4:1903–1905
Benson AJ (1968) Postrotational sensation and nystagmus as indicants of semicircular canal
function. In: Third symposium on the role of the vestibular organs in space exploration. Naval
Aerospace Medical Institute, Naval Aerospace Medical Center, Pensacola, FL, 24–26 Jan
1967. NASA SP 152, pp 421–432
Benson AJ, Goorney AB, Reason JT (1966) The effect of instructions upon post-rotational
sensations and nystagmus. Acta Otolaryngol 62:442
Birren JE, Fisher MB (1947) Susceptibility to seasickness: a questionnaire approach. J Appl
Physiol 31:288–297
Bles W, de Jong HAA, Oosterveld WJ (1984) Prediction of seasickness susceptibility. In: Motion
sickness: mechanisms, prediction, prevention and treatment. AGARD conference proceedings
No. 372, North Atlantic Treaty Organization Advisory Group for Aerospace Research and
Development, vol 27. Neuilly-sur-Seine, France, pp 1–6
Brown AC (1874) On the sense of rotation and the anatomy and physiology of the semicircular
canals of the internal ear. J Anat Physiol 8:327–331
Collins WE, Lentz JM (1977) Some psychological correlates of motion sickness susceptibility.
Aviat Space Environ Med 48(7):587–594
De Wit G (1953) Seasickness (motion sickness). A labyrinthological study. Acta Otolaryngologica
108(suppl):7–56
Dobie TG (1965) Motion sickness during flying training. In: AGARD conference proceedings
No. 2, North Atlantic Treaty Organization Advisory Group for Aerospace Research and
Development. Neuilly-sur-Seine, France, p 23
Dobie TG (1974) Airsickness in Aircrew. AGARDOGRAPH No. 177, North Atlantic Treaty
Organization Advisory Group for Aerospace Research and Development. Neuilly-sur-Seine,
France
Dobie TG (1980) An evaluation of the characteristics of repeat cupulograms and their relationship
to the subject’s flying experience and motion sickness susceptibility. In: Proceedings of the
annual scientific meeting of the Aerospace Medical Association. Aerospace Medical
Association, Washington, D.C., pp 183–184
Dobie TG (1981) The characteristics of multiple repeat cupulograms and their relationship to
flying experience, history of motion sickness and subsequent susceptibility to airsickness
during flying training. In: Proceedings of the annual scientific meeting of the Aerospace
Medical Association. Aerospace Medical Association, Washington, D.C., pp 201–202
Graybiel A, Wood CD, Miller EF II, Cramer DB (1968) Diagnostic criteria for grading the severity
of acute motion sickness. Aerosp Med 39:453–455
Hardacre LE, Kennedy RS (1965) Some issues in the development of a motion sickness
questionnaire for flight students. NSAM-916, US School of Aviation Medicine, Pensacola, FL
Hulk J, Jongkees LBW (1948) The turning test with small regulable stimuli. II. The normal
cupulogram. J Laryngol Otol 62:70–75
164
8 Prediction of Susceptibility to Motion Sickness
Hutchins CW, Kennedy RS (1965) The relationship between past history of motion sickness and
attrition from flight training. NSAM-932. US Naval School of Aviation Medicine, Pensacola,
FL
Kennedy RS, Dunlap WP, Fowlkes JE (1990) Prediction of motion sickness susceptibility. In:
Crampton GH (ed) Motion and space sickness. CRC Press Inc., Boca Raton, FL, pp 179–215
Lentz JM (1984) Laboratory tests of motion sickness susceptibility. In: Motion sickness:
mechanisms, prediction, prevention and treatment. AGARD conference proceedings No. 372,
North Atlantic Treaty Organization Advisory Group for Aerospace Research and
Development, vol 29. Neuilly-sur-Seine, France, pp 1–9
Miller EF, Graybiel A (1969) A standardized laboratory means of determining susceptibility to
Coriolis (motion) sickness. NAMI-1058, Naval Aerospace Medical Center, Pensacola, FL
Miller EF, Graybiel A (1970a) A provocative test for grading susceptibility to motion sickness
yielding a single numerical score. Acta Oto-laryngologica 5(274)
Miller EF, Graybiel A (1970b) Motion sickness produced by head movement as a function of
rotational velocity. Aerosp Med 41:1180–1184
Money KE (1970) Motion sickness. Physiol Rev 50:1–38
Morton G, Cipriani A, McEachern D (1947) Mechanism of motion sickness. Arch Neurol
Psychiatry. 57:58–70
Reschke MF (1990) Reliability of provocative tests of motion sickness susceptibility. In:
Crampton GH (ed) Motion and space sickness. CRC Press Inc., Boca Raton, FL
Turner M, Griffin MJ (1995) Motion sickness incidence during a round-the-world yacht race.
Aviat Space Environ Med 66:849–856
van Egmond AAJ, Groen JJ, Jongkees LBW (1948) The turning test with small regulable stimuli.
J Laryngol Otol 62:63–69
Chapter 9
Prevention of Motion Sickness
Abstract There are many and various ways that we can prevent, or at least reduce,
the likelihood and severity of motion sickness. We can start by avoiding exposure
to motion profiles that have been shown to be particularly provocative and in some
cases we can control the duration of exposure. We can also do our best to distract
those who are inexperienced travelers so that they are less likely to dwell on the
idea that they might become motion sick. As I have heard local sport fishermen say,
“If the fish are biting, I don’t get seasick!” Well-controlled increased exposure to
provocative motion together with supportive cognitive-behavioural training can go
a long way to helping people get their “sea legs” and adapt to other forms of
provocative motion on land, sea and in the air; I have been very successful in
training people to overcome their motion sickness, whatever the cause.
As Reason and Brand (1975) have pointed out, the scientific literature contains a
great variety of suggestions for preventing motion sickness and for managing the
problem once the symptoms have begun. They observed, however, that their study
of the Lancet, an authoritative medical journal, from 1829 until the end of the
century “revealed that practically everything that could be carried, worn or swallowed has been prescribed at one time or another.” Many of the drugs that had been
recommended bordered on the dangerous, particularly if the recipient had been
required to perform a complex or potentially hazardous task. In addition, however,
there are many other practical methods that are available for preventing or mitigating these motion sickness effects that are not only uncomfortable, but can also
produce serious
For example, Griffin (1996) has provided the following review of advice to ship
designers in his book on “Vibration”:
• “Oscillatory motion in the provocative range (0.1–0.5 Hz) should be measured
or predicted and the incidence of motion sickness estimated from dose-effect
data;
• At frequencies below 0.5 Hz, approximately, variations in translational acceleration due to changes in speed and direction and low frequency oscillation
should be minimised;
© Springer Nature Switzerland AG 2019
T. G. Dobie, Motion Sickness, Springer Series on Naval Architecture,
Marine Engineering, Shipbuilding and Shipping 6,
https://doi.org/10.1007/978-3-319-97493-4_9
165
166
9 Prevention of Motion Sickness
• Crewmembers should be located where low-frequency translational oscillation
is minimal around the centre of the ship;
• A clear view of distant objects should be provided wherever possible;
• Where practical, head support should be provided in order to reduce head
movements;
• Tasks should be designed that require the minimum of head and eye
movements;
• Try to avoid the use of optical devices that magnify or distort the visual field,
such as, binoculars and sights;
• Moving visual displays should not cause pursuit eye movements;
• Remember that an environment with constant speed rotation may cause balance
or motion sickness problems;
• Provide good environmental conditions onboard ships.”
Bittner and Guignard (1985) have also summarised methods of preventing or
mitigating the effect of ship motions on crewmembers, under five headings:
• “Ship Design and Systems Engineering—hull design; ship arrangements;
operation and maintenance of machinery and equipment; motion attenuation
device (e.g. fins); vibration isolation and damping treatments; isolation of special stations;
• Human Factors Engineering—arrangement and designs of crew space; location
and orientation of crew stations; work and task design; display control design
and placement; optimisation of ship environmental factors; individual
anti-vibration devices;
• Enhancing Natural Human Resistance to Motion Effects—optimisation of work/
rest and duty/leave cycles; habituation and oscillatory motion training; crew
selection; provision of adequate sleep;
• Modifying Adverse Physiological Reactions to Motion—optimisation of crew
fitness and morale; optimisation of the immediate physiological state;
medication;
• Operations Solutions:
Strategic and Tactical Planning to Minimise:
a.
b.
c.
d.
routing through rough motion areas;
distance/time spent in rough conditions;
number of units simultaneously exposed;
necessity to resupply in heavy seas.
Tactical Manoeuvering Compromises of:
a. speed;
b. heading;
c. stopping time at sea.
9 Prevention of Motion Sickness
167
I propose to address some of these issues under a number of headings, namely:
vehicular design; general measures; the mitigation of specific recipitating factors;
factors influencing habituation to motion; and the prevention of motion sickness by
means of vestibular training.
9.1
Vehicular Design
The design characteristics of particular vehicles, in terms of imposed frequency and
intensity of motion, can clearly influence the degree and character of the
provocative stimulation experienced by the crew and passengers (McCauley et al.
1976) and, in turn, determine the subjective responses. At the design stage of a new
project, these benefits can be achieved by altering the motion characteristics of the
vessel or vehicle in order to minimise exposure to accelerations known to be
provocative. This approach to providing protection can be taken a step further by
locating the critical working areas on the centre line of a ship, as near to the ship’s
centre of rotation as possible. It will also help to design workstations along the main
axes of the hull.
A similar approach is appropriate in flight where passengers will experience less
provocative stimulation when seated on the line of the wings of the aircraft. This
basic problem can be further improved by reducing the amount of head movement
made by an occupant, since head movements in a changing force field increase the
intensity of conflicting vestibular signals. During World War II, some
troop-carrying aircraft were fitted with special head rests so that a passenger’s head
has been restrained, thereby minimising head movements and the resultant induced
cross-coupled (Coriolis) vestibular accelerations (Johnson and Mayne 1953). The
design of seats and seat harnesses can also play a significant part in reducing active
head movements. It has also been suggested that a view of the outside world, and in
particular the horizon, can reduce motion sickness. I shall discuss this later in the
chapter.
9.2
General Measures
During their early experiences with provocative motion, many people suffer from
motion sickness or worry about the possibility of such an occurrence. In this frame
of mind they identify a whole variety of situations and apparent trigger mechanisms
as factors that cause their motion sickness (Dobie 1974). Education and reassurance
by supervisors, instructors or physicians can play a significant role in alleviating
these fears. In a working motion environment, good management is equally
important as a means of helping an individual through early experiences with
provocative motion (regardless of vehicle type) without suffering from motion
sickness.
168
9 Prevention of Motion Sickness
My early clinical observations at the RAF Aviation Medical Training Centre in
1963 have shown that arousal plays a very significant role in causing motion
sickness and many other distressing problems. This may be caused by exposure to a
form of provocative motion not experienced before, or occur during early exposure
to disturbing motion stimuli before adaptation has occurred. Among inexperienced
sailors or trainee aviators, another significant factor may be the fear of failing to
perform up to the standard that particular person wishes to achieve. Such an anxiety
overlay is a feature of a person’s level of motivation based on his or her personality.
It is not due to fear of some outside threat or agency.
Flight in large jet transport aircraft is less likely to provoke airsickness than
flying in a commuter or light aircraft. Modern wide-body aircraft do not usually fly
in turbulence for long periods, other than in clear air turbulence when calmer flight
levels are not available. On the other hand, fear of flying is a common cause of
airsickness among passengers who have little flight experience. This is less
prevalent among those who have chosen flying as a career. Anxious passengers
should be reassured and mentally diverted as much as possible. A similar situation
pertains to the provocative motion responses experienced on large cruise ships, as
compared to small sailing boats. In the latter case, the inexperienced passenger is
largely unoccupied and has little to think about other than the motion of the boat
and perhaps a previous bout of motion sickness
Personal Devices Used For Protection: The widespread use of so-called
anti-motion sickness devices is a striking indication of the commonly held
expectancy of becoming motion sick on a wide variety of conveyances. The
presence of a chain dangling from an automobile to provide a “ground” is an
example of one method used to try to prevent motion sickness, even though most of
the time the chain does not touch the road surface. Apparently there are others who
believe that they can protect themselves from the uncomfortable effects of
provocative motion by wearing a sheet of brown parcel paper on the surface of the
abdomen. Later we shall address the question of acupressure as a preventive
technique. Confidence in such procedures can be sufficient to protect a certain type
of person, but that individual remains vulnerable, particularly if he or she forgets to
use the appropriate talisman, or if it is not available.
State of Health: A person’s general state of health may also be significant. For
example, the prodromal symptoms of some diseases include nausea, and if this
occurs in a motion environment, it may lead to the incorrect assumption that it has
been caused by provocative motion. This is more likely to be associated with
isolated instances of so-called “motion sickness.” Also, over-indulgence in alcohol
during the evening prior to travel can be a cause of “vehicle sickness” and this may
well be labelled as motion sickness. This problem of erroneous labelling of the real
cause of sickness occurring during motion can in itself make some people believe,
incorrectly, that they are particularly prone to motion sickness.
Food Intake: Lindseth and Lindseth (1995) have studied the relationship of diet to
airsickness by examining the frequency and dietary content of meals in a population
of 57 novice civilian pilots. Regarding incidence, they found that 28% of all
these pilots reported airsickness. Six of the 8 female pilots have become airsick
9.2 General Measures
169
(75%) in comparison with only 10 of the 49 male pilots (20%). The dietary patterns
and food and nutrient consumption before flight were correlated with airsickness,
using a 24 h dietary survey. They found that foods high in sodium, such as preserved meats, corn chips, and potato chips, and foods high in thiamin, like pork,
beef, eggs, or fish showed a significant correlation with a higher incidence of
airsickness. Also they found that eating foods high in protein, for example, milk
products, cheeses, and preserved meat, correlated significantly with increased airsickness among the males. The frequency of meals eaten during the day also
correlated with increased airsickness. Of the pilots who had experienced airsickness, 50% consumed three or more meals in the previous 24 h, and 69% had eaten
within 6 h of flying. Four pilots fasted for the 24 h period or did not complete the
questionnaire. Higher density foods (more kilocalories) also increased the incidence
of airsickness in both the male and female pilots. Lindseth and Lindseth concluded
that eating food rich in carbohydrate just before flight seemed to reduce airsickness.
Stewart et al. (1989) have investigated 6 male and 1 female volunteers who were
exposed to stressful cross-coupled (Coriolis) stimulation in a rotating chair either
during a fasting state or following the ingestion of 6 ounces of yogurt. The subjects
were tested five times at weekly intervals. They found that those who have been
tested after eating yogurt reached a Malaise-III (see Table 6.1) endpoint of motion
sickness after significantly fewer head movements, and at lower rates of rotation
than those tested while fasting. The researchers noted that, although the ingestion of
yogurt increased a subject’s susceptibility to motion sickness, it did not affect the
pattern of the electrogastrogram. They did not know, however, whether this effect
was specific to yogurt, or a general response that would have been caused by
ingesting any substance that distended the alimentary canal. These workers have
postulated that in either case “the yogurt might influence central neural function
through little understood sensory receptors in the mucosa.” They also noted that
several subjects had not been keen to eat yogurt at room temperature, suggesting
that the prospect of ingesting an unappealing substance could in itself increase a
person’s susceptibility to motion sickness.
Uijtdehaage et al. (1992) have also investigated the effects of the ingestion of
food on the severity of motion sickness and the physiological mechanisms
involved. A total of 46 subjects who had fasted have been assigned either to a group
that was designated to be given food or to remain in a fasting state.
Electrogastrographic recordings were made before and after a meal and during
subsequent exposure to illusory self-motion in an optokinetic drum.
They found that the ingestion of food had inhibited the occurrence of the
symptoms of motion sickness. Subjects who were given a breakfast typical of their
choice have reported fewer symptoms during illusory self-motion than those who
fasted. They suggested that this result was in keeping with sailors’ folklore that
recommended eating before taking a boat trip. This would seem to contradict the
findings of Stewart et al. (1989), previously discussed, which have suggested that
eating yogurt at room-temperature increased a person’s susceptibility to motion
sickness. However, it is important to recognise that their test meal differed significantly with regard to type, attractiveness, and amount.
170
9 Prevention of Motion Sickness
People who are prone to motion sickness should avoid bulky, greasy meals,
particularly if there is little time to digest them before a journey begins. Feelings of
nausea associated with food may predispose someone to an attack of sickness
entirely unrelated to vehicular motion. Whereas, the frequent intake of light snacks
can be helpful to some people. It is interesting to note that Charles Darwin, the
famous naturalist, who has been particularly susceptible to seasickness, found that
raisins were “the only food that the stomach will bear” (Barlow 1946).
Effect of Odours: Many people are susceptible to foul odours and these may
produce nausea even in the absence of significant vestibular stimulation. The smell
of jet fuel and other engine fuels and lubricants has been cited in this context.
Similarly, the sight of another person vomiting can be disturbing and produce the
same response in the observer. Thus good ventilation in the passenger or crew
compartment, together with discreet management of those who are being sick, can
improve them and prevent onlookers being similarly affected.
9.3
The Mitigation of Specific Precipitating Factors
Passengers known to be susceptible to airsickness or who show signs of it should be
located in the most stable part of the vehicle. In aircraft this is usually a forward
position or one located on the line of the wings. In the case of ships it will be close
to the midline near the centre of the vessel, as mentioned under “Vehicular Design.”
In the case of automobiles, the front seats are invariably better. Since young children are required to ride in the back, for safety, it may help to position them so that
they have a relatively uninterrupted view ahead. This will reduce the need for them
to initiate additional provocative lateral head movements in order to see outside the
vehicle. In addition, it is wise to control early exposure to provocative motion so
that individuals do not experience unpleasant responses while they are adapting to
new provocative motion profiles.
Effect of Body Position and Visual Orientation: Tyler and Bard (1949) suggested
that the effects of body position and visual orientation could play a significant role
in the incidence of motion sickness in many cases. For example, Tyler (1946)
carried out a series of 24 experiments involving more than 2100 individuals during
amphibious operations approaching the shore on barges (Landing Craft Vehicle
Personnel). The troops were required to adopt different postures. In one condition,
they were made to crouch, resting on one knee, from the moment they entered the
barge and remain so for up to 3 h. This “ready” position had been adopted for
safety reasons so that the soldier’s head was below the gunwales. In the other
condition, under entirely comparable conditions otherwise, the troops were allowed
to stand in the barges until the last 10 min of the operation. The effect of body
position on the incidence of seasickness is shown in Table 9.1. Tyler believed that
the importance of this “visual factor” whereby one could see the horizon accounted
for the apparent protection shown by the reduction in seasickness. But it is also
9.3 The Mitigation of Specific Precipitating Factors
171
Table 9.1 The effect of body position on the incidence of seasickness
Body
position
Crouching
Standing
No. of
men
No. M. S.
No. S. S.
No. I. C.
Total
sick
Percent
S.S.
899
178
88
3
269
10.1
1220
116
26
1
143
2.2
Percent
sick
Range of
total sick
30
25–42
11.7
5–19
M.S. moderately sick, S.S. severely sick, I.C. incapacitated
possible that there was more head movement in the crouching position and less
stability, due to the lack of view.
Manning and Stewart (1949) have reported on a study in which they carried out
1005 swing experiments, involving 825 men, to investigate the effect of some 14
different body positions and visual orientation. The ropes that supported the 4-pole
swing were 14 feet in length and the frequency of swinging was 14 per minute. The
swing has been operated manually and they attempted to swing all the subjects
through an arc of 69°. They estimated that the swing error was small and represented a difference in angle of 2°. They have not attempted to control the time of
swinging in relation to eating since, in each group of subjects, it had been carried
out every 30 min throughout the day. The subjects were also required to maintain
the same bodily position in all of the experiments and kept the head in a constant
natural position without head restraint.
As can be seen in Table 9.2, there have been marked differences in the incidence
of motion sickness between the various groups, in terms of both body position and
visual orientation. The incidence was at its highest when the accelerative forces
were acting in the plane of the vertical semicircular canals. When the subjects were
lying in the supine position with their eyes open (group 1), the incidence of sickness
after swinging for 30 min was only 5%. In the sitting position with eyes open
(group 6), it rose to 27.5%. In group 7, however, when the subjects were swinging
in the seated position with their eyes closed, the sickness rate rose further to 51%.
When seated subjects with eyes open wore blackout goggles the incidence of
Type III swing sickness rose even further to 57.5%, whereas in a darkened room
with eyes open it dropped to 39%. On the other hand, when the subject was seated,
eyes open, in an enclosed cabin, completely isolated with no visual contact with an
ordinary stationary environment (group 11), both the incidence and severity
increased to a Type III swing sickness of 64%; the effect of the visual condition was
highly significant.
Manning and Stewart concluded that the highest incidence of swing sickness
took place in the seated position when the subject was enclosed in a cabin on the
platform of the swing. The least provocative of the 14 positions tested was the
supine position with the subject’s eyes open. They found that the overall group
incidence of motion sickness remained unchanged when the same subjects were
swung again after an interval of 7 days or longer. Within the group, however, there
were individual variations. Other factors, such as the time of day, meals, environmental temperature and apprehension appeared to have little or no effect on the
group results. They suggested that the adaptation of the supine position or another
172
9 Prevention of Motion Sickness
Table 9.2 Effect of posture on the incidence of swing sickness
Exptl.
group
nos.
1
2
3
4
5
6
Attitude of subject
and conditions
Eyes
open/
closed
Plane of
lateral
canal
Supine
Open
+107°
Supine (20 min)
Closed
+107°
Supine
Closed
+107°
Prone
Open
−40°
Prone
Closed
−40°
Sitting facing
Open
+21°
operator
7
Sitting facing
Closed
+21°
operator
8
Sitting facing
Open
+21°
operator—room dark
9
Sitting facing
Open
+21°
operator—with
goggles
10
Sitting facing
Open
+21°
operator—(Barany
Chair)
11
Sitting facing
Open
+21°
operator—swing
covered
12
Sitting side posn. on Open
+21°
chair
13
Sitting side posn. on Open
+21°
platform
14
Standing facing
Open
+11°
operator
Type 1 = No symptoms after 30 min. on swing
Type 2 = Pale & nauseated 30 min. on swing
Type 3 = Nausea and vomiting <30 min
No. of
men
Type
I (%)
Type
II (%)
Type
III
(%)
126
41
45
40
38
171
90
90
84.5
42.5
34
58.5
5
5
45
7.5
13
14
5
5
11
50
53
27.5
90
40
9
51
80
56
5
39
80
35
7.5
57.5
73
41
18
41
50
12
24
64
50
76
12
12
41
56
20
24
80
60
12.5
27.5
in which the vertical canals were horizontal might have a protective effect in
reducing the incidence of motion sickness when airborne troops were in transit to
the combat area.
Vogel et al. (1982) studied the hypothesis that otolithic stimulation caused by
linear acceleration when moving in a straight line was an effective stimulus for
causing motion sickness. They also compared the effect of different bodily positions, sitting (x-axis) and supine (z-axis) in terms of their effects on motion sickness
susceptibility. Thirty-eight volunteers (8 female and 30 male) aged 18–54 years
have been accelerated in a standard ambulance vehicle. The subjects were exposed
to weak forward acceleration alternating with brisk vehicular braking. The accelerations were recorded by means of a 3-axis linear accelerometer.
9.3 The Mitigation of Specific Precipitating Factors
173
They reported that their results clearly demonstrated that the horizontal linear
acceleration induced by their stop and go manoeuvres in the vehicle has effectively
produced motion sickness, in that 43% of the subjects have become motion sick in
less than 10 min of stimulation. They have also noted that a number of other
subjects who apparently have been free of motion sickness at the end of the
experiment became motion sick after a maximum of 20 min later. They also
reported that a further subject apparently free of sickness at the end of the test had
vomited some 30 min later when he was driving home. I have also noticed similar
latent responses in a number of the experiments that I have carried out in our
laboratory over the years involving Coriolis stimulation, either in our rotating/tilting
chair and also when following illusory motion in our optokinetic drum.
Vogel et al. also found that the incidence of motion sickness has been almost
twice as high in the seated position facing forwards as compared to lying supine. As
they pointed out, pure otolithic stimulation has already been shown to cause motion
sickness on parallel (four pole) swings and during constant speed barbecue spit
rotation.
Mills and Griffin (2000) have studied the effects of seat supports, the visual
environment and the direction of horizontal motion on the severity of motion
sickness on a horizontal vibrator. They used a total of 72 male subjects, aged from
18 to 25 years, assigned to 6 similarly aged and experienced groups of 12 subjects.
The effects of body position, vision and direction of motion were investigated in six
conditions. The subjects rated their motion illness response on a six-point rating
scale (Table 9.3). When the motion exposure ended, the subjects completed a
motion sickness symptomatology checklist.
They found that during fore-and-aft motion with eyes open and using the low
backrest, the illness ratings were significantly greater than with the high backrest.
During lateral motion, they found that the average illness ratings (eyes open) were
also higher with the lower backrest, but in this configuration they were not significant. In terms of the visual conditions, during both fore-and-aft and lateral
motion, the highest average illness ratings were reported during the eyes open
condition but not significantly so. In terms of the direction of motion, they found
that in the low backrest condition, the average illness ratings (eyes open and closed)
were higher during fore-and-aft motion when compared to lateral. That difference
had not been found to be significant, however. Mills and Griffin stated that these
Table 9.3 Mills and Griffin’s
six-point illness rating scale
Rating number
0
1
2
3
4
5
6
Adapted from Golding
Subjective feelings
No symptoms
Any symptoms, however slight
Mild symptoms, but no nausea
Mild nausea
Mild to moderate nausea
Moderate nausea but can continue
Moderate nausea and want to stop
and Kergulen (1992)
174
9 Prevention of Motion Sickness
results reflected greater head and upper body restraint while seated with a high
backrest, during fore-and-aft motion with eyes open since the high backrest, head
restraint and harness had been more effective in that direction rather than during
lateral motion.
Mills and Griffin concluded that the most nauseogenic conditions occurred when
the subject was seated with a low backrest, eyes open but with no external view for
fore-and-aft oscillation. On the other hand, the least nauseogenic condition was that
in which the subject had been seated, restrained, with a high backrest during fore
and aft oscillation.
Importance of Controlled Introduction to Provocative Motion: When passengers or trainees are on board an aircraft for the first time, it is important to minimise
motion stimuli by avoiding any unexpected or violent manoeuvres, since they are
not yet accustomed to flying. Ideally, a new aviator’s first few flights should be
limited to air experience, with gentle turns, aimed at stimulating his or her interest
in flying and allowing that person to enjoy the new sensation of flight. Kirkner has
made similar recommendations as long ago as 1948. It is also helpful for the
instructor to keep the inexperienced passenger interested by holding a conversation
with him or her and describing the surroundings, so as to keep that person fully
occupied. During this time, his or her level of habituation to vestibular stimuli will
start to increase. For that reason, acrobatic manoeuvres should be avoided, even if
requested, because the inexperienced passenger is not yet fully habituated to
provocative motion. In the early stages of training, flight crewmembers known to be
susceptible to airsickness should not be exposed to unexpected vestibular stimulation. This simply means that provocative manoeuvres that have not been included
in the pre-flight briefing should be avoided.
In the case of early experiences at sea, similar precautions can be taken.
Inexperienced passengers should not be invited for a trip when the water is particularly rough, since they will not have the opportunity to get their “sea-legs”
before feeling ill. In the case of inexperienced professional crewmembers that go to
sea in very rough weather, supervisors should keep them as busy as possible in
order to keep their thoughts off their stomachs. They should also be encouraged to
eat light meals often. An individual who is prone to motion sickness perhaps should
try to maintain visual orientation by fixating on the horizon or visible land whenever possible, as a means of reducing sensory mismatches. It should be pointed out,
however, that this anecdotal form of protection has not yet been fully investigated,
although preliminary results in our laboratory support the value of visual support.
Strong, reliable visual cues help to suppress conflicting cues from other sensory
modalities. Conversely, susceptible passengers below decks are better off keeping
their eyes closed wherever practicable when there is a likelihood of becoming
seasick. If possible, they should keep their minds busy or indulge in active conversation. However, one should bear in mind that reading commonly makes matters
worse. Also, head movements should be kept to the minimum for the reasons
already described. If practical, scheduling issues should be addressed in order to
avoid long periods between exposures to provocative motion, as discussed under
the heading, “Factors Influencing Habituation to Motion,” later in this chapter.
9.4 Benefit of Seeing the Horizon
9.4
175
Benefit of Seeing the Horizon
Wertheim et al. (1995) have reminded us that there is a lot of anecdotal evidence to
the effect that seeing the horizon suppresses seasickness. In that respect, Money
(1970) has opined that the use of appropriate visual information might reduce
motion sickness by as much as 50–90%. In an attempt to investigate this matter,
Wertheim and his colleagues have arranged to include the question “Could you see
the horizon from your work station?” in the NATO “Seasickness, Fatigue and
Performance Questionnaire” (PAQ) sponsored by Canada. This had given them an
opportunity to examine this issue during a sea trial on Hr. Ms. Tydeman. When they
examined the data from all 62 subjects, they did not identify any significant difference in the motion sickness ratings of those who had been able to see the horizon
during each “block” and those who had not (i.e., those going on duty at one o’clock
in the morning or at one o’clock in the afternoon). When they have split the subject
population into those who had been sick and those who had not been sick, some
interesting results have emerged. In the group of subjects who had been sick, the
motion sickness ratings decreased faster when the horizon had been visible; and
during the second voyage these subjects had not suffered further from seasickness.
Unfortunately, these researchers had been unable to carry out a valid statistical
analysis on the data since the number of scores larger than zero differed between
“blocks” and had been relatively small. For example, there had been only 12
subjects in the group who had become seasick. These workers have opined,
however, that adaptation becomes less specific to the particular motion profile of the
ship when the horizon is visible; although this seemed to be a relatively general
belief it required further investigation.
In our laboratory, we have carried out a preliminary investigation into the
anecdotal evidence that being on deck and able to see the horizon suppresses
seasickness. Our ship motion simulator (SMS) is housed in a large test cell and has
a split door so that the upper half of the door can be open or closed, while the lower
part remains closed for safety. The far end of the test cell, some 60 m from the
SMS, has a long horizontal bar conveniently placed to simulate a horizon. We
recorded each subject’s symptoms of motion sickness under two conditions;
namely, upper half open (on deck simulation) and the door fully closed (below deck
simulation) and have not found significant differences between these two conditions. In the “open” condition, the subject’s field of view has been somewhat
restricted [subtended visual angle = 42° (wide) and 45° (high)] and this restriction
requires further investigation. In addition, the subjects performed cognitive tasks on
a computer and this focus of attention may well have been protective, in terms of
reducing or preventing a motion sickness response.
176
9.5
9 Prevention of Motion Sickness
Use of an Artificial Horizon
Rolnick and Bles (1989) have investigated the possibility of preventing seasickness
by using a projected artificial horizon in front of an operator. Six male and 6 female
subjects, ranging in age from 20 to 26 years, were exposed to angular motion in a
tilting room under three different experimental conditions. The subjects have been
described as being oto-neurologically fit and not considered to be highly susceptible
to motion sickness. First, the subjects were seated in a closed cabin with the
windows covered and no external visual reference. In the second condition, the
windows were uncovered, thereby permitting a partial view of the outside world. In
the third condition, the windows were covered and a rotating laser beam has projected an artificial horizon on the internal walls of the room. Each experimental
condition lasted 30 min and there was an additional control condition with no
motion.
The subjects were required to perform head movements at each maximum tilt
angle of the room. These consisted of turning the head to the right sequentially,
through 45°, then extending the head over 45° to produce yaw and pitch-up and
finally, over to the 45° turn to the left producing yaw and pitch-down. Subjects were
also required to carry out two performance tests, composed of a Memory
Comparison Task and a Dual Task. The latter has consisted of a tracking task and a
Continuous Memory Task. The subjects completed a Motion Sickness
Questionnaire before the motion started and after each Continuous Memory Task.
The pre-motion symptom scores were subtracted from the total scores to provide a
“relative motion sickness score.” This is the format that my colleagues and I used in
the experiments described in Chap. 13. In addition, subjects were required to
provide ratings of their feeling of well-being between tasks. These ratings were
tabulated on a scale from 0 (very bad) to 100 (excellent).
None of the subjects experienced frank motion sickness, reaching a maximum of
M IIA (moderate malaise A) on the Graybiel scale (Table 6.1), however there was
an increase in the relative motion sickness score over time. Also, there was a
significant increase in motion sickness symptoms in the closed cabin condition as
compared to the uncovered windows and artificial horizon conditions. There was no
difference between the artificial horizon and windows. They found a reduction in
both the subjective rating of well-being and of performance over time. These effects
were particularly noticeable in the closed cabin condition. These workers concluded
that in terms of well-being ratings and relative motion sickness scores, the provision
of a visual reference had been beneficial. In terms of performance, however, the use
of an artificial horizon did not seem to prevent a decrement in performance when it
was compared to the closed cabin condition. Since the tilting room only provided
roll and pitch motion, Rolnick and Bles have stressed the need for further evaluation of the artificial horizon in conditions that included a major heave component
which is generally accepted to be the most nauseogenic condition.
Apart from the deleterious effects of motion sickness per se, the operational
efficiency of crewmembers can be seriously degraded by motion-induced
9.5 Use of an Artificial Horizon
177
interruptions (MIIs) caused by rough seas. These are physical disturbances that
affect an individual while standing or walking on a moving platform and interfere
with one’s ability to carry out physical and perhaps cognitive tasks. While studying
this problem on the NBDL six degrees of freedom motion platform in our lab., we
observed that the lack of an external visual reference has made the problem worse.
In order to investigate this matter further the frequency of MIIs has been recorded
under conditions that have and have not provided subjects with a view of the
outside world. This has been achieved by installing black curtains attached to the
guardrail on the outer edge of the motion platform and suitable lighting for each
condition. When the curtains were in place on the handrail of the platform the
subject was unable to see the walls of the room in which the platform has been
installed.
Each subject carried out a number of standing and walking tasks on the moving
platform on two separate occasions; starting with or without an external visual
reference followed by the reverse order on the second exposure, completely
counterbalanced for each group (males and females). In addition to scoring MIIs by
two independent observers, force plate data have also been collected in the standing
conditions. The results have indicated that the subjects experienced more MIIs
when the installed curtains excluded an external visual reference. This showed that
an external reference was supportive in terms of improving postural stability on the
moving platform. This finding has suggested that the provision of visual displays,
as a replacement in compartments that did not permit a view of the real world could
be beneficial. The improved postural stability would not only improve performance,
but it would also reduce the likelihood of the occurrence of accidents and might
also reduce the incidence of motion sickness (Dobie et al. 2003).
9.6
Factors Influencing Habituation to Motion
For most people, repeated or continued exposure to motion over a few days reduces
susceptibility to motion sickness. A state of habituation builds up in response to
repeated vestibular stimulation (Guedry 1965; Graybiel et al. 1969) and then decays
if exposure to provocative motion is not continued over a period of time, which can
vary from a few days to some six to ten weeks. supervisors should bear this in mind
when they schedule inexperienced crewmembers. Flight instructors should not
expose trainees to strongly provocative manoeuvres during their first sortie after a
layoff. Long periods without reinforcing stimulating manoeuvres should be avoided
wherever practicable. For example, an occasional acrobatic manoeuvre at the end of
a navigational exercise should be included if this is possible and compatible with
the aircraft type and efficiency of that training sortie. The student will then be less
likely to lose his or her level of habituation during that early phase of training.
Similarly, people learning to sail should try to have regular lessons until they
become experienced, after which a break in continuity is less likely to create a
problem, because they have gained in confidence as well as gaining their “sea legs.”
178
9.7
9 Prevention of Motion Sickness
Prevention of Motion Sickness by Vestibular Training
Ground-based “vestibular exercises” may help some people habituate to motion and
maintain that state (Popov 1943); Kirkner made a similar suggestion in 1948. This
can be achieved by means of gymnastic exercises that stimulate the vestibular
apparatus (e.g., by tumbling and rolling on an exercise mat, or by using sophisticated gymnastic equipment, such as a trampoline.”)
After the selection approach had failed to predict a candidate’s susceptibility to
motion sickness, I considered using a form of preventive physical training based on
vestibular training, as described by Popov (1943). In that programme, persons with
increased vestibular sensitivity would be given periods of training lasting from 2 to
24 days, using the so-called “double test with rotation,” which Voyachek (1943)
had proposed for investigating the function of the vestibular apparatus. The subject
would be seated in a Bárány chair, eyes closed, and his head inclined forward at an
angle of approximately 90°. He was then rotated for ten seconds in either direction
at the rate of one turn every two seconds, for a total of five revolutions. The chair
was then stopped and the subject maintained his position for a further five seconds.
He was then asked to open his eyes and sit upright. While straightening up, the
trunk and head has tended to incline in the direction of rotation. In different individuals, these so-called “protective movements” might be absent altogether, or
expressed as mild, average, or strong, in proportion to the “effect exerted by the
otolithic apparatus on the function of the semicircular canals.” During training, they
found that these “protective movements” had become weaker with practice and
reported that they had been able to suppress the reaction in 13 out of 18 subjects.
Unfortunately, however, no follow-up information has been provided as to how
well these candidates have coped with provocative motion during flight training, so
that matter is still to be tested..
For subjects who had exhibited particular “vestibular sensitivity” during flight
training, they provided a course of “vestibular training.” In addition to the double
test procedure, they added active vestibular gymnastics and swinging on four-pole
swings. I began preventive physical training in the RAF (without the swing);
however, such training meant using time allocated to the physical fitness programme that would also have meant giving this type of training to all student
aircrew, since, as previously stated, attempts to identify motion-susceptible students
had been unsuccessful. This preventive approach was unacceptable to the training
organisation, however, because their physical training hours were tightly controlled
and since no guarantee of a successful outcome could be given at that stage, it had
to be cancelled. That left me with no alternative but to turn my attention to
managing those trainees who suffered from severe motion sickness during flight
training in some other way.
In the late 1950s and early 1960s, I successfully developed a cognitivebehavioural desensitization training programme using repeated exposure to
increasing Coriolis vestibular accelerations over a period of days, together with
some confidence-building support to manage severe motion sickness. This new
9.7 Prevention of Motion Sickness by Vestibular Training
179
anti-motion sickness training programme is discussed later in some detail in
Chap. 12. At a later date, others used that type of approach but without the cognitive component (Dowd 1964). However, I believe that the efficacy of this type of
training is greatly enhanced when combined with an augmented form of psychological de-conditioning, as will be discussed in detail later, when reviewing the
history and rationale of my training programme in Chap. 12. As we shall see, the
inclusion of counselling to deal with the arousal present in chronic severe motion
sickness is a particularly important feature.
The subject of cognitive-behavioural training deserves further investigation,
however. The concept of reducing crew sizes in the new designs of ships means that
maximum crew efficiency is a critical issue. Since cognitive-behavioural training
has proven to be very successful in managing motion sickness, I believe that the
addition of a cognitive component to a preventive physical training programme
would enhance its effectiveness and that is another issue that should be pursued.
9.8
Factors Related to Simulator Sickness
There are many helpful means of alleviating simulator sickness and these form part
of flight simulator training syllabi in many organizations. For example, Kennedy
et al. (1987) have prepared guidelines for alleviating the symptoms of simulator
sickness and these have been published as a field manual for students and instructors
by the Naval Training Systems Center. The following is a summary of these recommendations, together with some additions from Money (1991) based on his own
experience with flight simulator sickness in the Aurora CB140FDS (Money 1980).
General Rules:
• Pilots should be aware of the time course of simulator sickness symptomatology. Those most at risk are those who are new to the simulator and those with
extensive flight time but little simulator experience;
• Remember that first exposure to the simulator is more provocative than later
sessions, and that certain types of simulation are also more provocative than
others;
• Adaptation is one of the strongest means of overcoming the problem. So one
should try to achieve optimal adaptation to the simulator by flying it on a daily
basis but do not go beyond the level of moderate nausea;
• Avoid flying the simulator on the same day as flying the actual aircraft;
• Avoid stressful conflict by entering the simulator and settling down before
turning on the visual display;
• Timeouts should be used frequently;
• In training scenarios that are particularly nauseogenic, one should plan to make
the periods of exposure shorter and the number of timeouts should be increased;
• Simulator training should only be performed by those who are in their usual
high state of fitness; and finally,
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9 Prevention of Motion Sickness
• When fully adapted to the simulator, do not discard all of these rules because
they may still introduce a sickness response.
Simulation Flight Scenarios:
• Minimise as far as possible the number of turns during taxiing or normal flying;
• Reduce, as much as possible, close interaction with the ground;
• Minimise rapid alterations in attitude and altitude and relatively violent
manoeuvres;
• Head movement should be reduced as much as possible, particularly in the
nodding plane, especially when moving scenes are being demonstrated;
• Try to concentrate on instrument flying, rather than visual, in cloudy conditions;
• In terms of shipboard landings, it is recommended to initiate these with zero sea
state since it is more nauseogenic when the sea state is high;
• Freeze conditions, or resetting the simulation, should be avoided during early
exposure. If they do occur, instructors should take over and fly out of the
conditions;
• Avoid slewing while the visual is on. When problems arise, it may be worth
considering turning off the motion base;
• During initial exposure to simulation, it might be advisable to reduce the size of
the visual field;
• During breaks and seat changes, the scene should be turned off and ambient
light turned on, particularly before leaving the simulator; and
• Those with a history of motion sickness should be treated as novice pilots during
their early simulator training.
Engineering and Maintenance Tuidelines:
• It is important to ensure that all the computer-generated cameras are correctly
aligned; and
• The following problems should be reported:
–
–
–
–
Changes in stick response;
Distorted visual colour balance;
Movements of the motion base which are not initiated;
Any misalignment between and within displays.
Instructor Guidelines:
• Instructors should be familiar with this condition so they are better able to
manage their subjects;
• Try to avoid creating simulator sickness by suggestion; and
• Minimise whatever is thought to cause simulator sickness.
In conclusion, I feel strongly that the management of trainees during simulator
training is critically important so as to prevent the occurrence of simulator sickness
in the first place. This approach is similar to that which I have already suggested
regarding the introduction of beginners to sailing and flying and indeed any other
9.8 Factors Related to Simulator Sickness
181
form of provocative motion. However, overemphasis on the possibility of suffering
from simulator sickness can evoke these responses. Unless these rules are used
judiciously, it is likely that the arousal that can be provoked may make matters
worse. It is of paramount importance that instructors make every effort to try to
avoid creating simulator sickness by suggestion.
9.9
Summary
• Key factors in the prevention of motion sickness include vehicular design,
general measures, mitigation of specific precipitating factors, factors influencing
habituation to motion, and vestibular training.
• A subject’s state of mind may affect the severity of motion sickness symptoms.
I have stated that education and reassurance by supervisors or instructors can
play a role in alleviating subject’s fear and anxiety.
• Specific precipitating factors can reduce motion sickness symptoms such as
body position, lying on one’s back with eyes open, and visual orientation,
keeping one’s eyes on the horizon. In terms of virtual displays to replace the
actual horizon, this last option is still under investigation and requires careful
investigation lest the display itself causes motion sickness.
• A state of habituation develops through repeated or continued exposure to
motion and this reduces susceptibility to motion sickness. Vestibular training
may be useful to habituate some individuals to provocative motion and may well
be optimal with a cognitive component.
• Turning to the advisory notes regarding the alleviation of simulator sickness, I
would recommend that this information be used by supervisors to plan and
manage the training sessions, rather than leaving it to the student. This positive
approach will reduce the likelihood of inducing motion sickness by suggestion.
References
Barlow LN (ed) (1946) Charles darwin and the voyage of the beagle. Philosophical Library, New
York
Bittner AC, Guignard JC (1985) Human factors engineering principles for minimizing ship motion
effects. Naval Eng J 97(4):205
Dobie TG (1974) Airsickness in aircrew. AGARDOGRAPH No. 177, North atlantic treaty
organization advisory group for aerospace research and development, Neuilly-sur-Seine,
France
Dobie TG, May JG, Flanagan MB (2003) The influence of visual reference on stance and walking
on a moving surface. Aviat Space Environ Med 74:838–845
Dowd PJ (1964) Induction of resistance to motion sickness through repeated exposure to Coriolis
stimulation. SAM-TR-64-87, USAF School of Aerospace Medicine, Brooks AFB, TX
182
9 Prevention of Motion Sickness
Golding JF, Kerguelen M (1992) A comparison of the nauseogenic potential of low-frequency
vertical versus horizontal linear oscillation. Aviat Space Environ Med 63:491–497
Graybiel A, Dean FR, Colehour JK (1969) Prevention of overt motion sickness by incremental
exposure to otherwise highly stressful Coriolis accelerations. Aerosp Med 40:142–148
Griffin MJ (1996) Handbook of human vibration. Academic Press Ltd., London (paper back
edition)
Guedry FE Jr (1965) Habituation to complex vestibular stimulation in man: transfer and retention
of effects from twelve days of rotation at 10 rpm. Percept Mot Skills 21:459–481
Johnson WH, Mayne JW (1953) Stimulus required to produce motion sickness: restriction of head
movement as a preventative of airsickness—field studies onairborne troops. J Aviat Med 24
(400–411):452
Kennedy RS, Berbaum KS, Lilienthal MG, Dunlap WP, Mulligan BE, Funaro JF (1987)
Guidelines for alleviation of simulator sickness symptomatology. Orlando, FL: Naval Training
Systems Center, NAVTRASYSCEN TR-87-007
Lindseth G, Lindseth PD (1995) The relationship of diet to airsickness. Aviat Space Environ Med
66:537–541
Manning GW, Stewart WG (1949) Effect of body position on incidence of motion sickness. J Appl
Physiol I(9):619–628
McCauley ME, Royal JW, Wylie CD, O’Hanlon JF, Mackie RR (1976) Motion sickness
incidence: exploratory studies of habituation, pitch and roll, and the refinement of a
mathematical model. Tech. Report No. 1733–2, Human Factors Research, Incorporated, Santa
Barbara Research Park, Goleta, CA
Mills KL, Griffin MJ (2000) Effect of seating, vision and direction of horizontal oscillation on
motion sickness. Aviat Space Environ Med 71:996–1002
Money KE (1970) Motion sickness. Physiol Rev 50:1–38
Money KE (1980) Flight simulator sickness in the Aurora CP140 FDS. DCIEM technical
communication No. 80-C-44
Money KE (1991) Simulator sickness. In: Motion sickness: significance in aerospace operations
and prophylaxis. AGARD-LS-175. NATO/AGARD, Neuilly-sur-Seine. 6B,1–4
Popov AP (1943) Special vestibular training. In: Voyachek WE, Kulikovsky GG,
Rosenbloom DE, Vishnevsky NA (eds) Steiman I. trans, fundamentals of aviation medicine.
University of Toronto Press, Toronto, Canada
Reason JT, Brand JJ (1975) Motion sickness. Academic Press, New York, NY
Rolnick A, Bles W (1989) Performance and well-being under tilting conditions: the effects of
visual reference and artificial horizon. Aviat Space Environ Med 60:779–785
Stewart JJ, Wood MJ, Wood CD (1989) Electrogastrograms during motion sickness in fasted and
fed subjects. Aviat Space Environ Med 60:214–217
Tyler DB (1946) Influence of placebo, body position and medication on motion sickness. Am J
Physiol 146:450–466
Tyler DB, Bard P (1949) Motion sickness. Physiol Rev 311–369
Uijtdehaage SHJ, Stern RM, Koch KL (1992) Effects of eating on vection-induced motion
sickness, vagal tone, and gastric myoelectric activity. Psychophysiology 29(2):193–201
Vogel H, Kohlhaas R, von Baumgarten RJ (1982) Dependence of motion sickness in automobiles
on the direction of linear acceleration. Eur J Physiol 48:399–405
Voyachek WE (1943) Double test with rotation. In: Voyachek WE, Kulikovsky GG,
Rosenbloom DE, Vishnevsky NA (eds) Steiman I. trans, Fundamentals of aviation medicine.
University of Toronto Press, Toronto, Canada
Wertheim AH, de Groene GJ, Ooms J (1995) Seasickness and performance measures aboard the
Hr. Ms. Tydeman. TNO Report TNO-TM, TNO Human Factors Research Institute,
Soesterberg, NL
Chapter 10
Pharmacological Treatment of Motion
Sickness
Abstract Practically everything has been tried at one time or another to treat
motion sickness. There are a number of medications that are quite effective,
although most have some unwanted side effects and some adversely affect performance. Scopolamine and promethazine are still considered to be the most
effective anti-motion sickness medications. Perhaps the most disturbing feature of
the anti-motion sickness drug story is that nothing new and effective has appeared
in the last forty years or so. Recently, drugs that have effective anti-emetic properties in certain clinical settings have not been found to be effective in a motion
environment. If you are treating passengers, make your choice of medication
according to circumstances such as duration and severity of exposure and individual
idiosyncrasies. When dealing with operators of potentially hazardous equipment or
those performing certain skilled tasks, the choice is more difficult and it may be
better to avoid drugs all together.
The most common method of treating motion sickness is the use of one of the many
different anti-motion sickness drugs currently available, or even a placebo.
A suitable anti-motion sickness drug, or combination of drugs, should prevent or
reduce the effects of motion sickness. Both the time to peak therapeutic activity and
the duration of action should be known. Regarding therapeutic effectiveness,
Lawther and Griffin (1988) have reported the results of a survey in which they
found that 26% of over 2000 passengers on sea-going ferries had taken anti-motion
sickness medication on that voyage. Notably, 11.4% of those who took anti-motion
sickness medication vomited during the trip, compared with only 5.6% of those
passengers who took no medication at all. Nieuwenhuijsen (1958) has investigated
the use of anti-seasickness drugs among 193 passengers, of whom 119 became
seasick on a trans-Atlantic crossing in heavy weather, and reported the following:
• of a total of 50 males who did not take anti-motion sickness drugs, 13 (26%)
became seasick;
• of 30 females who did not take these drugs, 14 (47%) became seasick;
• of a total of 30 males who did take drugs, 22 (73%) became seasick;
• of 83 females who took anti-seasickness medications, 70 (84%) became seasick.
© Springer Nature Switzerland AG 2019
T. G. Dobie, Motion Sickness, Springer Series on Naval Architecture,
Marine Engineering, Shipbuilding and Shipping 6,
https://doi.org/10.1007/978-3-319-97493-4_10
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However, as Nieuwenhuijsen pointed out, one must remember that those who
took medication have been expecting to become sick and the drugs may also have
been taken too late to be effective.
Brand and Perry (1966) published a valuable review of the methods used to
study drugs used in the management of motion sickness. In their introduction, they
have stated that “in all this body of information, there is a singular lack of cohesion
and many of the findings are apparently irreconcilable.” They surveyed the methods
that have been used to study these pharmacological agents under three main
headings, namely, field trials in man, laboratory methods in man and laboratory
methods in animals. They have carefully tabulated all these types of experiments
and tried to separate what they deemed to be facts from supposition and speculation. It had been their hope that their review document would provide helpful
directions for future work in this field.
Brand and Perry concluded that the only valid way to determine the effectiveness
of a pharmacological compound in treating motion sickness was to test it in a
“properly designed field study in man.” They did admit that this statement avoids
the complex issue of what actually comprises such a study and pointed out that
most of the experimental work that they had reviewed has avoided that question
also. They summarised this matter according to the underlying situational
requirement for the medication. They have proposed that if the drug is required to
treat established motion sickness or to prevent this malady in people already
exposed to provocative motion, the primary consideration is the speed of onset of
its action. If, however, one was faced with the problem of transferring healthy
troops from a delivery vehicle to land after a short exposure to very severe motion,
the main concerns should be that the drug was highly effective and free of side
effects. On the other hand, if the requirement was simply one of making prolonged
sea voyages more pleasant for the individual, the main requirement was for the
medication to provide a lengthy duration of action so as to reduce the frequency of
dosages. These factors clearly dictate the experimental design under which the
drugs should be studied so as to recognise the situation in which they are to be used.
Brand and Perry’s observations on the effectiveness of specific drugs in treating
motion sickness are addressed later in this chapter.
In general, the medication of choice should not have any side effects that are
uncomfortable or potentially hazardous to health, and additionally for the worker,
should not be detrimental to that individual’s ability to work safely and efficiently.
This also means that we need to know how individuals respond to the selected
standard dosage of that particular drug. In many ways, this is much more of a
problem than merely finding drugs that exhibit protective effects. In the context of
protecting professionals, both at sea and in the air, the physician must balance the
effectiveness of a particular compound, and its side effects, against the needs of the
person and the tasks to be performed. For this reason it is essential that the
physician in charge strictly controls the use of anti-motion sickness medication. It is
a medical responsibility to ensure that the user does not exhibit personal idiosyncrasies to the particular drug and that he or she is fully aware of the likelihood and
nature of any unwanted effects.
10
Pharmacological Treatment of Motion Sickness
185
The situation is quite different with passengers. In their case, the choice of an
anti-motion sickness drug is very much the result of personal preference, or the
power of advertising. The unwanted effects of the drug of choice are much less
serious when the recipient is a passenger, because the question of skilled performance is not usually relevant. For example, a sedative action may be a positive
advantage in such cases. Similarly, prolonged use of drugs is less likely to occur,
because a passenger’s flights or sea voyages are usually less frequent and fairly
isolated in time. On the other hand, this means that passengers usually begin each
trip in a virtually unhabituated state from the point of view of susceptibility to
motion sickness. In addition, passengers who rely on medications usually have a
serious problem when they forget them, because their oversight results in increased
arousal.
Belladonna alkaloids have been among the earliest drugs to be used in the
treatment of motion sickness. According to Tyler and Bard (1949), they were first
suggested anonymously in 1869 for this purpose. These drugs are widely found in
nature, especially in the Solanaceae plants. The alkaloid atropine is found in deadly
nightshade (Atropa belladonna) and the alkaloid scopolamine (hyoscine) mainly in
the shrubs of Hyocyamus Niger and Scopolia canniolica. Atropine and scopolamine
are both organic esters. They are competitive antagonists of the action of acetylcholine and other muscarinic agonists. These two drugs differ quantitatively in their
antimuscarinic actions, particularly in terms of their effect on the central nervous
system (CNS). Atropine has little or no effect on the CNS, whereas scopolamine has
significant effects, even at low doses, perhaps due to its greater ability to cross the
blood-brain barrier.
I shall now discuss the pros and cons of some commonly used medications for
the treatment of motion sickness. However, I should point out that this is not
intended to be a comprehensive treatise on the pharmacology of such medications.
However, in addition to a number of excellent review articles to which I shall refer,
there are also many comprehensive pharmacological books available for those who
have a special interest in the pharmacokinetics and pharmacodynamics of these
compounds, which are beyond the scope of this text.
10.1
Scopolamine (Hyoscine Hydrobromide)
Scopolamine, an antimuscarinic, is probably the single most effective anti-motion
sickness drug, but suffers the drawback of producing considerable side effects.
During World War II, Holling et al. (1944) has noted that a number of drugs had
been investigated in order to evaluate their ability to prevent seasickness among
troops and that hyoscine (0.6 and 1.2 mg) had appeared to be the most generally
successful. This is still true today. Lucot (1998) has reported that scopolomine is
not selective in terms of the 5 types of muscarinic receptors found in the living
body. The adult oral dose of 0.3–0.6 mg is readily absorbed from the gastrointestinal tract, reaches peak effectiveness after 30–60 min, and lasts about four
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hours. Glaser and Hervey (1952) have reported that scopolomine (1 mg) is effective
in reducing the nausea and vomiting of experimental seasickness when given 5–
10 min before the onset of provocative motion, but is even more effective when
given 1¼ h beforehand. Because long motion exposures require repeated doses,
oral scopolamine is best suited for short exposures to provocative motion (Stott
1991). An oral dose of 0.6 mg of scopolamine produces side effects consisting of
dryness of the mouth, dizziness, light-headedness, and drowsiness. A reduction in
pursuit performance scores has been reported, but this has been restored with the
addition of 5–10 mg of d-amphetamine (Wood et al. 1985). However, this solution
has its own drawbacks, as we shall see later. Repeated doses are not recommended
for patients with glaucoma or prostatic enlargement (Wood 1990). In 1974, I carried
out a crossed-over, double-blind trial to investigate the unwanted effects of 0.5 mg
scopolamine and different dose levels of trimethobenzamide in 100 flight trainees,
and found that five subjects gave unsolicited reports of visual disturbances after the
ingestion of scopolamine. No such reports followed the ingestion of either the
placebo or trimethobenzamide.
Uijtdehaage et al. (1993) have examined the effects of scopolamine on subjects’
physiological responses before and during the motion sickness responses induced
by circular vection in an optokinetic drum. In particular, they have investigated
cardiac vagal tone by recording respiratory cardiac arrhythmia, and measured heart
rate and electrogastrogram (EGG) activity. They also examined the use of physiological profiles as predictors of motion sickness. Sixty male college students have
each ingested 0.6 mg scopolamine, 2.5 mg methscopolamine, or a placebo. In
comparison with the other groups, the scopolamine group reported fewer symptoms
of motion sickness, and exhibited a lower heart rate, higher vagal tone, increased
normal gastric myoelectric activity, and reduced gastric dysrhythmias. These results
had been obtained both before and during the induction of motion sickness, by
means of illusory motion in the optokinetic drum. These authors reported that
certain base-line physiological patterns obtained prior to provocative stimulation
could identify those subjects who would develop gastric discomfort. On the other
hand, subjects who would remain free of symptoms had been characterised by high
levels of vagal tone and low heart rate across conditions, and by maintaining the
normal 3 cpm electrogastrographic activity during the period of exposure to illusory
motion. Uijtdehaage et al. concluded that scopolamine offered protection against
motion sickness induced by visually-induced apparent motion by initiating a particular pattern of increased vagal tone, enhanced gastric myoelectric activity, and
suppressed tachyarrhythmia similar to the control subjects who have not suffered
from stomach discomfort or nausea.
Scopolamine has been shown to impair vigilance and short-term memory
(Brazell et al. 1989). Golding et al. (1988) reported that scopolamine (1.2 mg)
significantly impaired performance on a variety of mental and motor tasks, altered
focal length, lowered heart rate, and produced dry mouth, headache, and dizziness.
The Physicians Desk Reference (2000) has given a comprehensive and precise
summary of the potential problems that may be associated with ordinary therapeutic
doses of scopolamine.
10.1
Scopolamine (Hyoscine Hydrobromide)
187
The Physician’s Desk Reference states:
Since drowsiness, disorientation, and confusion may occur with the use of scopolamine,
patients should be warned of the possibility and cautioned against engaging in activities that
require mental alertness, such as driving a motor vehicle or operating dangerous machinery.
Rarely, idiosyncratic reactions may occur with ordinary therapeutic doses of scopolamine.
The most serious of these that have been reported are: acute toxic psychosis, including
confusion, agitation, rambling speech, hallucinations, paranoid behaviors, and delusions.
Payne et al. (1952) have studied the effects of certain motion sickness preventives on psychological efficiency. They pointed out that ideally one would study
these effects in flight in order to compare aviation skills in the control and drug
groups, matched for in-flight experience and proficiency. However, this ideal scenario was not practical at the time and they adopted an indirect alternative using a
comprehensive battery of psychological tests in a laboratory setting.
In the study, Payne and his colleagues included hyoscine alone, a combination of
diphenhydramine (Benadryl®) and hyoscine, (Benadryl®) alone and dimenhydrinate (Dramamine®) alone. In general they found that these drugs caused a decrement in test performance. In addition, they concluded that the drugs have the
greatest effects on those psychological functions that are highly implicit, such as
visual imagery, ideation, mental set and judgment. The least effects were found in
those explicit tests such as perceptual-motor and spatial activities. In their opinion,
this distinction corresponded with the main psychological differences between
piloting and navigational duties and that the drugs have a more profound effect on
navigational rather than piloting proficiency. Their ultimate conclusion has been
that the decision to use anti-motion sickness drugs, or not, forces a choice between
two undesirable alternatives and that the requirement for a palliative without performance deficit seems best satisfied by scopolamine.
In the following year, Payne et al. (1953) specifically addressed the issue of the
effects of anti-motion sickness drugs on navigator efficiency. In that study, they
included hyoscine, benadryl/hyoscine, promethazine (Phenergan®), and a mixture
of all three drugs. They concluded that 0.65 mg scopolamine (hyoscine) showed
little, if any, behavioral evidence to preclude its use in what they called
“run-of-the-mill” navigational missions, assuming that is, that there were no
unacceptable idiosyncratic responses. Today’s tasks are significantly more complex
than in 1953, but it is interesting to consider their comments concerning the types of
tasks most affected by these medications. Much later, Fleishman and Quaintance
(1984) developed this concept of evaluating performance from the standpoint of
human abilities. Fleishman’s taxonomy provides analysis tools that permit operational duties and tasks to be described in a structured manner.
Holling et al. (1944) had investigated the side effects of scopolamine in a military setting in an effort to prevent seasickness in troops about to land on a hostile
shore. They selected hyoscyamine, atropine and scopolamine and carried out the
trials at sea. Out of a total of 212 men who had been given the placebo tablets, 90
(42.5%) vomited and a further 9 (4%) had become nauseated, giving a total of 99
(46.5%) described as seasick. On the other hand, of those who had been given
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0.6 mg of scopolamine, only 31 (14%) vomited and a further 13 (6%) had become
nauseated, bringing the total number of subjects experiencing seasickness to 44
(20%). Holling et al. have stated that the only unpleasant side effects with scopolamine were reported by those who had been given the higher dose of 1.2 mg of the
drug. Judging by the date of that publication, the work had no doubt been prompted
by the forthcoming D-Day landings. As I reported at the beginning of the first
chapter, motion sickness was a major problem for the forces heading for the beaches of Normandy.
Regan and Ramsey (1996) investigated the effectiveness of scopolamine in
reducing the symptoms of motion sickness caused by the simulation of a suite of
rooms and their contents by means of virtual reality. There had been 39 subjects in
the study, 33 males and 6 females. Subjects were given the same experimental
directives to ensure, as much as was possible, that each person experienced similar
exposure to this virtual world. In a double-blind study, with placebo, a dose of
300 µg of scopolamine was given to 19 subjects and a placebo to a further 20
subjects, 40 min before exposure to a 20 min immersion in virtual reality. The
severity of subjects’ motion sickness had been obtained by means of a commonly
used simulator sickness 27 item symptomatology checklist, and a 6-point self-rating
malaise scale. They carried out a 2 2 Chi-square analysis in order to compare the
number of subjects who had reported some symptoms of motion sickness, that is to
say greater than 1 on the self-rating scale, in the scopolamine and placebo groups.
This demonstrated a statistically significant reduction of motion sickness in the
scopolamine group. Regan and Ramsey concluded that scopolamine caused a
significant reduction in the symptoms of motion sickness commonly found when
people were immersed in a virtual environment. This is perhaps a predictable
outcome on the basis that this form of simulator sickness is still a condition that we
know as “motion sickness” and scopolamine is a very effective anti-motion sickness
agent.
Kohl et al. (1986) have pointed out that, since the early 1970s when first used in
the Skylab programme, the most commonly used anti-motion sickness medication
for reducing the symptoms of the Space Adaptation Syndrome has been a combination of 0.3 mg of scopolamine and 5 mg of d-amphetamine. They also reported
that the drug combination of second choice was 25 mg of promethazine
(Phenergan®) combined with ephedrine (50 mg). Both of these prophylactic mixtures contain sympathomimetic drugs. These agents are frequent constituents of
anti-motion sickness drug combinations because they are useful in overcoming the
sedative effects caused by stressful motion or resulting from the administration of
other anti-motion sickness drugs. Although the effectiveness of scopolamine can be
increased by combining it with amphetamine; as will be seen later, this is achieved
at a price.
Schmedtje et al. (1988) have also examined the effects of these two drugs,
scopolamine and dextroamphetamine, as a means of preventing motion sickness.
They used dosages appropriate to their operational environment in space and
measured human performance using five computer-based tests of both cognitive
and psychomotor skills, namely, symbol-digit substitution, simple reaction time,
10.1
Scopolamine (Hyoscine Hydrobromide)
189
pattern recognition, digit span memory, and pattern memory. Each of the 8 subjects
had been given the tests in the same order during each session. Prior to this study
there have been reports of decrements in human performance during similar performance tests, but in these cases higher dosages of scopolamine or dextroamphetamine had been used. These researchers used a combined dose level of 0.4 mg
oral scopolamine and 5.0 mg oral dextroamphetamine that was being used in the
space programme at that time, and were unable to detect any decrement in
performance.
In that series, there has been one case where there was a possible trend toward
reduced performance with scopolamine, however this has been reversed when
dextroamphetamine was added to scopolamine in combination. Schmedtje et al.
acknowledged that these ground-based tests were perhaps not realistic measures of
the effects of the drugs in space because of other possible effects on both the
pharmacokinetics and pharmacodynamics of the drugs due to microgravity. They
also stressed that they did not investigate the effects of repeated doses, which could
alter the side effects. This, as discussed later, is similar to the observation by
Oosterveld et al. (1972) that drugs should be tested in conditions similar to those in
which they are to be used.
Kennedy et al. (1990c) conducted a study to gain experience with the Automated
Performance Test System (APTS) and attempted to confirm and extend those
results published by Schmedtje et al. (1988), which have just been discussed.
The APTS consists of standard mental acuity tests with the advantages that stability
occurred within 3 experimental trials; there was a high level of reliability; the test
exposures were brief; and it was factorially rich.
Oral scopolamine (1.0 mg) and d-amphetamine (10 mg) were administered,
alone and together, to 2 groups of 8 subjects, randomly assigned to the test sessions
in a crossed-over within-subjects design. After reaching test stability, the subjects
performed the 9 tests on a portable microcomputer in the double-blind design
during four weekly drug treatments, including a placebo. These workers reported
different effects on performance. Motor and perceptual speed tests seemed to have
improved under the action of d-amphetamine and have not been degraded by
scopolamine. Two of the 5 cognitive tests, namely, pattern comparison and
grammatical reasoning, showed reductions with scopolamine. On the other hand,
d-amphetamine generally improved subjective performance on speed-based tests
that emphasised motor skills including speed of information processing. The
combination of scopolamine and d-amphetamine improved performance on motor
tasks compared with the placebo group. They also related these effects of scopolamine in both this study, and previous studies elsewhere, in the form of a model
that implied that the reduction in performance depended upon whether it was
cognitive, motor, or self-reporting, as well as on the amount of medication taken.
Based on that model, Kennedy et al. (1990c) summarised their conclusions as
follows: below a dose of 0.15 mg, scopolamine has no effect on performance;
below 0.50 mg, the decrement is limited, but can be demonstrated by certain
sensitive and complex performance tests and self-reports; above an oral dose of
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1.0 mg, however, the severity of the reduction in performance is likely to affect
operational efficiency.
Wood et al. (1985) have also evaluated the side effects of anti-motion sickness
drugs on performance. They used a computerised pursuit meter, which had been
shown to have a high correlation with operational performance (Evans et al. 1973).
It consisted of a 15 in. Videotek colour TV monitor, a Radio Shack TRS 80 colour
computer and a TRS 80 printer. Lower total error scores indicated improved performance. The study was conducted as a conventional double-blind, crossed-over,
Latin square design with placebo, with 10 subjects in each study. The subjects
consisted of both males and females with ages ranging from 18 to 30 years.
Their results have shown that the pursuit performance scores were improved
over placebo in subjects who ingested d-amphetamine (10 mg and 5 mg); also with
a combination of promethazine (25 mg), scopolamine (0.4 mg), and
d-amphetamine (10 mg), and finally, the combination of scopolamine (1 mg) with
d-amphetamine (10 mg). However, the pursuit performance scores were not significantly different from the placebo scores in those tests where the subjects have
been given scopolamine (0.25 mg, 0.5 mg, or 0.6 mg); marezine (50 mg); meclizine (50 mg); or dimenhydrinate (50 mg). This outcome has also been obtained
with drug mixtures containing scopolamine (1 mg) with d-amphetamine (5 mg.);
and promethazine (25 mg) with d-amphetamine (10 mg). On the other hand, they
obtained a significant reduction in the performance scores with 1 and 0.8 mg
dosages of scopolamine, and with 25 mg dosages of promethazine, whether given
orally or intravenously. In addition, they found significant reductions in performance scores, compared with placebo, when subjects ingested either a mixture of
promethazine (25 mg) with scopolamine (0.4 mg), or a combination of promethazine (25 mg oral plus 25 mg I.M.) with d-amphetamine (10 mg). Wood and his
colleagues concluded that anti-motion sickness drugs could be used without loss of
operational proficiency when the dosages and combinations of drugs were carefully
selected.
In the following year, Wood et al. (1986) turned their attention to the effect of
scopolamine and d-amphetamine on habituation. They rotated 12 subjects, both
male and female, aged between 18 and 30 years, once a day for five days up to the
malaise III (Table 6.1 in Chap. 6) end-point, using cross-coupled (Coriolis) stimulation. This has been achieved by means of active head movements during rotation
on a Contraves Goerz chair equipped with limiting head rests at the front, back and
on each side. The test medications were administered to the subjects using a
modified Latin square design in a double-blind study with placebo. The effectiveness of each of the drugs has been evaluated by the subject’s response to
provocative stimulation using the step-test method (Graybiel and Knepton 1977).
The subjects made 40 head movements at each rotational speed, starting at 1 rpm
and increasing by 2 rpm increments to a maximum of 35 rpm, depending on the
subject’s end-point. The experimental drugs that have been given before each test
exposure were a placebo, 1 mg of scopolamine, 10 mg of d-amphetamine, or a
combination of 0.6 mg of scopolamine with 5 mg of d-amphetamine.
10.1
Scopolamine (Hyoscine Hydrobromide)
191
With the placebo, the 12 subjects averaged only 48 more head movements over
weeks 2–5, than they had previously performed during the initial untreated test
exposures. The placebo scores have a Spearman coefficient correlation of 0.88 with
the initial untreated tests. This denoted that there has been a high reliability for the
M-III end-point and that little habituation has taken place due to the experimental
design. The fastest rate of habituation has taken place with a combination of 0.6 mg
of scopolamine with 5 mg of d-amphetamine, and the 1 mg dose of scopolamine
was only slightly slower. The 10 mg dose of d-amphetamine has also demonstrated
an increase in habituation over placebo. When the test medications have been
stopped on day 5, however, the experimenters noted that there had been a rebound
in sensitivity to cross-coupled (Coriolis) vestibular stimulation with both scopolamine alone and with the scopolamine/d-amphetamine mixture. Wood et al. (1986)
concluded that during rotation, habituation proceeded when the subjects were given
scopolamine and amphetamine. They suggested that this increase in habituation to
Coriolis stimulation seemed to be a result of the medications allowing subjects to
withstand the provocative motion for a longer time. However, there was a rebound
effect when the scopolamine was withdrawn, causing a marked decline in tolerance
to provocative motion. They suggested that this was due to “increased activity of
the cholinergic neurons.”
Kennedy et al. (1966) noted that many depressant side effects of scopolamine
(hyoscine) and meclizine could be offset by combining them with d-amphetamine
and many of the stimulant effects of d-amphetamine could be overcome with the
addition of a depressant. In addition, they found that it was necessary to use both
questionnaire and psychomotor methods in order to obtain a fuller measure of these
side effects.
Buccal Tablets Containing Scopolamine: Golding et al. (1991) have pointed
out that the length of time that a particular anti-motion sickness drug, or combination of drugs, is effective, depends upon both the speed of absorption and the
subsequent elimination of the medication. This caused them to investigate whether
or not scopolamine could be absorbed more rapidly in the form of buccal tablets
allowed to dissolve in the mouth, when compared to the standard oral variety that
have been swallowed. In the United Kingdom, where they carried out the study,
buccal scopolamine is available over the counter and is known as Kwells®. There
were 10 fit male experimental volunteers in the study, with a mean age of
33.9 years (S.D. ± 3.6), each of whom has taken either buccal or standard oral
tablets, both containing 0.6 mg of scopolamine hydrobromide, on two different
occasions. In all subjects, blood samples of 10 mL each were obtained at 0, 5, 15,
30, 45, 60, 75, 90, 120, 180 and 240 min following administration of the tablets,
and the plasma scopolamine levels were measured using a radio receptor assay of
these samples. Further blood samples were also made available from another 8
volunteers who had ingested a pharmacy-prepared scopolamine capsule also containing 0.6 mg of scopolamine hydrobromide.
Their results indicated that there were no significant differences in the overall
mean levels of scopolamine in the plasma between the two routes of absorption and
no statistically significant advantage in terms of speed of action for the buccal
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tablet. However, they found that the time to peak plasma time for the buccal tablet
has been, as one might expect, related to how quickly it dissolved in the mouth. The
mean time to peak levels was approximately 50 min. They also found that there was
a great individual variation in the speed of absorption of scopolamine and rate of
elimination. The mean half-life was approximately 170 min. They suggested that
this could account for the fact that some people fail to obtain protection from
motion sickness despite taking their medication. The information from an additional
8 subjects who had consumed the 0.6 mg scopolamine capsules was also compared
with those data obtained from the 10 subjects who had ingested the standard tablets.
Although a point-to-point comparison has not been possible due to different sampling times, the peak scopolamine levels were not significantly different. Golding
et al. (1991) noted, however, that individual plasma scopolamine levels tended to be
more consistent with the buccal tablet. They also found that the ingestion of a light
breakfast an hour before taking a scopolamine capsule did not slow absorption
when compared with a subject who had fasted. Although these results did not show
significant differences between the buccal and the oral route, the buccal route might
still have some advantages in the emergency situation. An ingested tablet is likely
to be ejected during emesis, whereas a survivor might be able to trap the tablet
under the tongue or behind the lip when vomiting. In any case, he or she would
likely know if the medication had been lost.
Norfleet et al. (1992) investigated the effectiveness of 1 mg of scopolamine
hydrobromide, placed in the subject’s buccal pouch, for treating motion sickness
induced by parabolic flight manoeuvres. Twenty-one male subjects, between 19 and
51 years of age, were exposed to these manoeuvres aboard a KC-135 aircraft. Each
subject has taken part in 2 flights, one after ingesting scopolamine and the other, a
placebo. On the first flight, 11 subjects took the medication and the remainder, the
placebo, in a random crossed-over experimental design. The subject’s second flight
with the other tablet was at least 1 week later. During the flights, the subjects were
exposed to periods of 0/G for 20 s, 2 G for 25 s, 1 G for 15 s, and 1.8 G for 25 s.
During each parabola, an investigator, who was blind to the content of the tablets,
recorded the subjects’ signs and symptoms of motion sickness.
Those subjects who had been treated with buccal scopolamine showed a significant reduction in scores for nausea, of between 31 and 35%, compared with
flights using the placebo. In addition, the subjects taking scopolamine also showed
a reduction of 50% in terms of the number of parabolas during which they have
vomited. The side effects of buccal scopolamine during flight were considered to
have been negligible. Norfleet et al. concluded that buccal scopolamine was more
effective than a placebo in treating motion sickness during parabolic flight
manoeuvres. In addition, they reported the further advantage that, unlike the oral
preparation, the subject could withhold the medication until the onset of symptoms.
Transdermal Patch Containing Scopolamine: A transdermal patch containing
scopolamine has been developed for longer motion exposures, such as sea voyages
lasting more than 24 h. The Transderm Scop® system is a circular flat disc designed
for the continuous release of the drug when it is applied to an area of intact skin
behind the ear. This patch contains 1.5 mg of scopolamine and is designed to
10.1
Scopolamine (Hyoscine Hydrobromide)
193
deliver 0.5 mg of the drug, at an approximately constant rate, over the three-day life
of the system, but may not be suitable for children (Wood 1990). An effective drug
concentration is not achieved until some six to eight hours after the patch is applied
(Stott 1991). This delay can be reduced to one hour or less by the simultaneous
administration of a single dose of oral or buccal scopolamine (Golding et al. 1991).
With the scopolamine patch, between four and six-fold variations in urinary
excretion rates have been reported (Stott 1991). Other studies have shown variability in drug response between subjects (Pyykko et al. 1985). After removal of the
patch, excretion of the drug has continued for up to 48 h, which probably indicated
that active amounts of the drug remained in the skin at the site of the patch (Schmitt
and Shaw 1981) and this has to be borne in mind when repeated patches are being
used.
While agreeing that scopolamine was the most effective single drug for the
prevention and treatment of motion sickness, Parrott (1989) pointed out that the
duration of action of both oral and injected scopolamine was relatively short, being
of the order 5–6 h. In addition, as already pointed out, scopolamine caused
potentially serious side effects on the autonomic and central nervous systems. The
newer transdermal scopolamine patch system, designed to deliver the drug over a
longer 72-h period, was mainly intended to reduce these problems.
Transdermal scopolamine does indeed provide significant protection against
motion sickness, similar to that provided by oral scopolamine or to a lesser extent
dimenhydrinate (Dramamine®). Despite the longer delivery time, however, the
scopolamine patch causes adverse effects on the autonomic nervous system consisting of dryness of the mouth, slowing of the heart rate, and blurring of vision due
to reduced visual accommodation. Repeated applications of these patches increase
the visual problems and this is particularly serious for people who are farsighted
(hypermetropes). The effects on the central nervous system consist of reduced
memory for new information, an impairment of attention, and reduced alertness.
Parrott has also pointed out that there are differences both in individual responses to
transdermal scopolamine as well as to different patch applications on the same
person. He summarised the main advantages of this patch as ease of use and
extended period of action. The main disadvantages are the lengthy lead time, some
6–8 h, which is necessary before starting exposure to provocative motion (suggesting the need for an oral or buccal loading dose), the adverse visual responses,
and the variations in the action of the drug by this route.
Noy et al. (1984) compared the effectiveness of transdermally administered
scopolamine (TTSS) with that of oral dimenhydrinate (Dramamine®) and a placebo,
in preventing motion sickness at sea. The 140 male subjects, aged 18–25 years,
were divided into four groups, and received the following combinations of drugs:
TTS scopolamine and dimenhydrinate placebo (28 subjects); TTS scopolamine
placebo and dimenhydrinate (30 subjects); TTS scopolamine placebo and dimenhydrinate placebo (30 subjects); and a control group (52 crew members), in a
controlled, double-blind study. They found that a placebo effect, perhaps associated
with other factors, reduced the incidence of motion sickness from 57.7% in the
control group to 43.5%. Dimenhydrinate reduced the incidence of motion sickness
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to 22.2% and TTS scopolamine, has further reduced that figure to 16.7%. In
summary, Noy et al. reported that the transdermal therapeutic system scopolamine
(TTSS) provided 61.7% protection against seasickness, compared to 48.9% with
dimenhydrinate and 24.6% for the placebo group. These authors suggested that
TTSS would be the best choice for most ships’ crews.
Pyykko et al. (1985) have also evaluated the therapeutic effects of
TTS-scopolamine and dimenhydrinate on motion sickness using 16 healthy subjects
aged between 21 and 38 years. In addition, they included lidocaine and tocainide,
and studied the effects on vertigo, and caloric and post-rotatory nystagmus, as well
as motion. Lidocaine was introduced in 1948 and is a widely used local analgesic.
Tocainide is a primary amine analog of lidocaine, which has been developed more
recently and whose properties are the same as lidocaine. Local analgesia has also
been used to treat vertigo and nausea. Tocainide can be given orally since it passes
the intestinal barrier.
Nausea has been induced by means of pseudo-Coriolis illusory stimulation in an
optokinetic drum. Vertigo was induced by means of a clinical caloric test in a
recumbent subject whose head has been supported at 30°, eyes open, in a dark
room. The subject’s left ear was irrigated with 350 mL of water at 30 °C for 90 s.
The subject was required to assess any illusion of self-motion on a scale of 1–100.
Binocular eye movements were recorded electrooculographically in the horizontal
plane. The rotational test was carried out with the subject seated in a chair accelerating within 1 s to a speed of 120°/s, followed 1 min later by a deceleration to a
stop within 1 s. This test was conducted when the subject’s eyes had been open in
the dark and the programme was designed to calculate the characteristics of the
induced nystagmus.
TTS-scopolamine was administered to subjects transdermally by means of 2
patches applied behind the ear and programmed to deliver approximately 10 µg/h
scopolamine base. The patches were applied 12 h before each test. Dimenhydrinate
(100 mg) was administered orally by capsule, and lidocaine and tocainide were
infused via the cubital vein (constant plasma concentration on average of lidocaine
6 mol/L and of tocainide 20 mol/L). In these randomly controlled tests, both
TTS-scopolamine and dimenhydrinate significantly reduced the vertigo which was
induced by caloric stimulation of the ears; the nausea which has been produced by
the pseudo-Coriolis illusory stimulation; and nystagmus. However, neither lidocaine nor tocainide reduced vertigo, and nausea was present. These drugs reduced
nystagmus induced by caloric stimulation but did not reduce nystagmus induced by
pseudo-Coriolis stimulation. Pyyko et al. presumed that TTS-scopolamine and
dimenhydrinate acted at the level of the brain stem and have their target cells in the
vestibular nuclei; the lessening of motion sickness was also associated with a
decline in nystagmus. On the other hand, it was noted that neither lidocaine nor
tocainide, which were thought to control vertigo and nausea by their action on the
vestibular end organs and the supratentorial brain structures, reduced the level of
motion sickness during these experimental exposures.
Gordon et al. (1986) investigated the effect of transdermal scopolamine on
human performance, using 23 enlisted naval volunteers aged between 18 and
10.1
Scopolamine (Hyoscine Hydrobromide)
195
20 years. The transdermal therapeutic system for scopolamine (TTSS) and the
placebo have been in identical form and both the TTSS and placebo patches were
placed behind the ear. The study was conducted over 3 different days separated by
an interval of one week. The first day involved training and on the night before the
second experimental day, the subjects were randomly assigned to one or other
group, receiving either TTSS scopolamine or a placebo patch. On the third and last
experimental day, the conditions were reversed. The test battery was divided into 3
groups, as follows: a battery of professional naval related tests, cognitive tests, and
measures of side effects of the medication. The professional tests included vigilance, tracking, Morse tests, and a navigational plotting task. The cognitive tests
were composed of code substitution, number comparison, together with arithmetic,
visual search, and auditory digit span tests. The evaluation of side effects included a
visual test, measures of salivation, and a mood state questionnaire. Gordon et al.
concluded that the administration of transdermal scopolamine had not caused a
significant decrement in performance and could be used safely by naval crews.
Workers from the same laboratory (Attias et al. 1987) continued the study of
transdermal scopolamine during sea trials on a 3,000-ton vessel sailing for 72 h in
the Mediterranean Sea. The sea states were as follows: day 1, sea state 3, and days 2
and 3, sea state 2–3. They tested 38 male volunteers, whose ages ranged between 20
and 25 years old. They used Graybiel’s diagnostic criteria (Table 6.1 in Chap. 6) to
calculate the percent of protection on the basis of seasickness defined as malaise II
or greater (Miller and Graybiel 1970a). They found that the drug provided 74, 73,
and 39% protection during the three sailing days, respectively. Based on a second
questionnaire at the end of the trip, the apparent drop in protection on the third day
had been due to the reduction in the number of subjects in the placebo group who
had been sick. There were no significant differences in the magnitude of the side
effects between the experimental and placebo groups. These workers concluded that
the protection against seasickness afforded by transdermal scopolamine during a
three-day cruise has not been associated with significant side effects. They decided,
therefore, that the results obtained during these sea trials have confirmed their
previous laboratory investigation and that the TTSS patch was suitable for
long-term use by ship’s crews.
Wang et al. (1992) investigated the relationship between the development of
motion sickness, together with the associated levels of histamine and
5-hydroxytryptamine (5-HT), and the mechanisms of the anti-motion sickness
action of the transdermal therapeutic system of scopolamine (TTTS). This study
included 10 healthy subjects, 9 males and 1 female, aged between 23 and 28 years.
Provocative (Coriolis) stimulation was induced by active forward and backward
head movements during bodily rotation within an optokinetic drum. The subjects
had given a magnitude estimate of their motion sickness response on a scale of 0–
100, during the three tests. The first test without drugs provided the control level.
Before the second and third provocative tests, a subject was either given scopolamine or a placebo in a double-blind crossed-over, randomised study. The blood
levels of histamine and (5-HT) have been measured by the fluorometric method,
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following the induction of motion sickness by exposure to cross-coupled (Coriolis)
stimulation.
The results showed that the mean motion sickness scores recorded in three
cross-coupled (Coriolis) tests were lowest in the group using transdermal scopolamine. With or without the administration of transdermal scopolamine (TTSS), the
results showed that the levels of histamine in the blood increased significantly
following motion sickness and were even higher in subjects receiving scopolamine
(TTSS). However, these researchers did not find any significant changes in the
blood levels of 5-HT following motion sickness, and there were no significant
differences in these blood levels between the transdermal placebo and scopolamine
groups. They decided, therefore, that there might not be a relationship between
5-HT and the onset of motion sickness. Wang et al. concluded that histamine was
involved in the development of motion sickness, and that the anti-motion sickness
protection which has been provided by scopolamine might involve its action on the
central or peripheral histaminergic systems, as well as the acetylcholinergic system.
Low-dose of Intra-Nasal Scopolamine: In 2010, Simmons et al. pointed out
that although oral and transdermal scopolamine were effective as anti-motion
sickness drugs they were absorbed somewhat slowly; for that reason they decided to
investigate INSCOP which is an intranasal form of scopolamine. So each of the 16
volunteers in the study was given 0.4 mg. Dosage of intranasal lNSCOP and a
placebo in a randomised double-blind crossover design. After 40 min the subjects
experienced exposure to Coriolis cross-coupling, in a staircase design, until they
reached a state of moderate nausea. During that period of testing, data were collected concerning the effectiveness of the drug and measures of any side effects of
physiological, cognitive and measures of their state of awareness. Overall, they felt
that the drug was very effective in dealing with the motion
They decided that the intranasal delivery of scopolamine seemed to offer a
promising alternative to the current oral and transdermal approaches without cognitive problems or increased side effects. As a result a gel form of INSCOP was
made and tested under an agreement between Johnson and the Naval Aerospce
Medical Research Laboratory in Pensacola Florida.
10.2
Antihistamines
Lucot (1998) has pointed out that, although they are less effective than antimuscarinic drugs, antihistamines are used more commonly in the clinical management
of motion sickness. These drugs are safer, have fewer side effects apart from
drowsiness, and are active over a longer time. Some of the antihistamines, such as
promethazine (Phenergan®) and dimenhydrinate (Dramamine®) also have anticholinergic properties.
Promethazine (Phenergan®): Promethazine, an H1-receptor antagonist (antihistamine), is the only phenothiazine that has been proven to be effective against
motion sickness. Since scopolamine has been shown to be the most effective drug
10.2
Antihistamines
197
for preventing motion sickness, this suggests that the anticholinergic properties of
certain H1 antagonists may account for their anti-motion sickness effects. An oral
dose of 25 mg of promethazine has been only slightly less effective than 0.6 mg of
scopolamine. Its onset of effectiveness begins some 2 h after ingestion, and its
duration of action has been quoted as low as 6 h (Wood 1990) and as long as 18 h
(Stott 1991). Marked sedation and dryness of the mouth have been associated with
this drug. In a retrospective analysis of 94 first flight crewmembers, Jennings et al.
(1993) reported that intramuscular promethazine has decreased the symptoms of
space motion sickness.
In an experiment to study various anti-motion sickness drugs Paul et al. (2005)
found that promethazine 25 mg. and d-amphetamine 10 mg did not reduce performance nor increase sleepiness. Whereas, Estrada et al. (2007) found that
promethazine 25 mg. plus caffeine 200 mg. showed a reduction in airsickness and
fewer side effects for military passengers in a Black Hawk helicopter. Weerts et al.
(2014) also carried out a similar study and promethazine 25 mg. plus
d-amphetamine 10 mg. did not affect any of the cognitive functions, but many of
the side-effects, including sleepiness, were reported.
Glaser and Hervey (1952) compared different dosages of promethazine
hydrochloride and l-hyoscine hydrobromide (scopolamine) to prevent nausea and
vomiting in army volunteers exposed to artificial wave motion while seated on
inflatable rubber floats in a large swimming pool. They found that promethazine
hydrochloride (35 mg) prevented nausea and vomiting in fewer subjects than either
scopolamine (1 mg) or scopolamine (0.6 mg) in combination with promethazine
(15 mg). However, the results have proven inconclusive when they compared
scopolamine with combinations of scopolamine and promethazine.
Wood et al. (1965) reviewed various anti-motion sickness medications in use
during the period 1954–1964. They classified promethazine as either a tranquiliser
or an antihistamine. In that review, they stated that extensive testing of the drug has
shown it to be an effective remedy, with 78% effectiveness, as compared with 90%
for scopolamine. In view of its reported sedative action, they concluded that it had
limited usefulness as an anti-motion sickness drug. As we know, NASA favors the
use of promethazine by astronauts on current space shuttle missions, typically on
the first day of the mission and before going to sleep (Putcha et al. 1999). They
have also observed that intramuscular (IM) administration (25 mg or 50 mg doses)
appeared to be the most effective route. NASA scientists have further investigated
the use of IM promethazine and its possible effects on human performance. This
study is discussed later in this chapter under the heading “Intramuscular Injection of
Medication.” They have further reported that drowsiness has been the only side
effect associated with its use and this has been limited to 25% of those who had
taken an intramuscular dose of the drug. By taking the drug before going to sleep,
however, this is not such a disadvantage.
Dimenhydrinate (Dramamine®): Dimenhydrinate, an ethanolamine, is another
first generation H1-receptor antagonist. A number of antihistamines are popular for
the prevention of motion sickness; of these, dimenhydrinate seems to be the most
effective (Wood 1990). It is a nonprescription drug that works satisfactorily in
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moderately provocative motion environments. Like other antihistamines, however,
the adult dose of 50 mg of dimenhydrinate produces some drowsiness and mild
dizziness as side effects.
Cyclizine Hydrochloride (Marezine®): Cyclizine hydrochloride, a piperazine, is
another H1-receptor antagonist used for protection against motion sickness. Its
duration of action is some 4–6 h for a single adult dose of 50 mg. Although this
antihistamine is less effective than dimenhydrinate, it also produces milder side
effects, such as drowsiness and dizziness. Weinstein and Stern (1997) have compared the effects of cyclizine and dimenhydrinate in motion sickness induced by
illusory motion in an optokinetic drum. In that study, they noted that 30 min after
the ingestion of cyclizine, subjects had experienced significantly less drowsiness in
the absence of provocative motion than they had after dimenhydrinate. After
16 min of rotation in the optokinetic drum, however, greater drowsiness had been
experienced with cyclizine than with dimenhydrinate. As they pointed out, however, drowsiness is both a symptom of motion sickness as well as a side effect of
these drugs, so they could not identify the cause of this effect in that particular
study.
Brand et al. (1965) compared 2 doses of scopolamine (0.1 and 0.7 mg of the
base) with 5 different dosages of cyclizine hydrochloride (15, 25, 40, 65 and
100 mg), in a study involving 500 naval volunteer subjects during exposure to
provocative motion in life rafts in an artificial wave pool. They found that detailed
dose/response curves for cyclizine paralleled those for scopolamine. They also
noted that dosages of scopolamine as low as 0.1 mg of the base have effectively
protected 75% of susceptible volunteers and produced no effects on vision and only
a small incidence of dryness of the mouth. It is also interesting to note that out of 58
volunteers who had received the placebo, 21 (36%) experienced giddiness; 31
(53%) experienced sleepiness; 16 (28%) experienced dryness of the mouth; and 10
(17%) had experienced blurred vision. On the other hand, in the group that had been
given 0.7 mg of scopolamine, only 8 (14%) experienced headache; 11 (19%)
experienced giddiness; 39 (68%) experienced sleepiness; 40 (70%) reported dryness
of the mouth; and 9 (17%) had experienced blurred vision. Cyclizine hydrochloride
has been recommended as a good choice of medication for the prevention of motion
sickness in children and has no restrictions in terms of usage during pregnancy
(Wood 1990).
Meclizine Hydrochloride (Antivert®, Bonine®): Meclizine is also a piperazine
used in the management of motion sickness. However, unlike the other antihistamines already mentioned, its rate of onset is slower and the duration of action is
longer (Wood 1990). For example, the duration of action across the single adult
dose range of 12.5–50 mg is 12–24 h, in comparison with 4–6 h for the 50-mg
single adult dose that has been reported for cyclizine (Hardman et al. 1996). It has
been suggested that this extended duration of action could be advantageous for the
prevention of motion sickness during longer journeys. Meclizine is not recommended for children under 12 years of age, nor is it recommended during pregnancy (PDR 2000).
10.2
Antihistamines
199
Cinnarizine (Stugeron®): Cinnarizine is also a weak antihistamine (piperazine
derivative) and in addition has some calcium antagonist properties. According to
Pingree and Pethybridge (1989), cinnarizine and hyoscine hydrobromide (scopolamine) are the drugs most commonly used in the British Royal Navy for protection
against motion sickness. In that service, apparently, the demand for cinnarizine is
about ten times greater than it is for scopolamine. These workers have reported that
an oral dose of 30 mg cinnarizine given 5 h before exposure to provocative
cross-coupled (Coriolis) motion showed statistically significant protection, compared with placebo. Golding et al. (1988) investigated the effects of the drug on task
performance and concluded that at oral dosages of 30 and 75 mg, cinnarizine was
well tolerated. It has also been found to be relatively free of significant side effects.
At present cinnarizine does not have FDA approval for use in the United States.
Doweck et al. (1994) carried out a controlled study to evaluate the anti-motion
sickness protective effect of two different doses of cinnarizine in heavy sea states.
Ninety-five healthy male naval crewmembers, aged 18–30 years, were divided into
three randomly selected groups that received: two 25 mg tablets of cinnarizine
(50 mg dose); one placebo tablet plus one 25 mg tablet of cinnarizine; or two
placebo tablets, respectively. The subject’s susceptibility to seasickness was evaluated on a 0–7 point scale by means of a standard questionnaire based on the
subject’s motion sickness responses during previous sea voyages in what they
considered to be normal sea conditions (mid-way between calm and rough) (Wiker
et al. 1979). The severity of the subject’s seasickness has then been evaluated
immediately after a 4–6 h voyage in very rough seas with 3.5 m waves, using the
same questionnaire. Possible side effects of the test drug were also recorded by
means of the subject’s responses to a four-point scale, ranging from 0, denoting no
side effects, through mild (1), moderate (2), to severe (3).
Doweck et al. found that of the 31 subjects who had taken 50 mg of cinnarizine,
20 of them felt less seasick than on previous voyages (65%). This figure was greater
than the 41% of subjects (10 out of 32) who received 25 mg of cinnarizine and the
31% of the 32 subjects who were given the placebo. The seasickness susceptibility
scores for the group that received the 50 mg of cinnarizine were significantly lower
than the placebo group. Protection at the lower dosage of 25 mg of cinnarizine was
not, however, statistically greater than the placebo. There were no significant side
effects recorded for any of the drug groups. Therefore, these particular workers
concluded that as an anti-motion sickness drug, 50 mg of cinnarizine was effective
in preventing seasickness in heavy seas.
Pingree and Pethybridge (1994) compared the effectiveness of cinnarizine as an
anti-motion sickness agent against that of scopolamine, in a double-blind sea trial
involving 179 crewmembers from two frigates, (89 on HMS Argonaut and 90 on
HMS Nottingham). These researchers had planned the trial with a crossover design
on each ship, and medication was given to the test subjects on a prophylactic basis
when weather information indicated the likelihood of rough seas. The motion of the
ship was recorded during those periods when the subjects were receiving
anti-motion sickness medication. On one ship (HMS Argonaut), moderate to severe
provocative motion had been encountered and a parallel groups trial had been
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performed. On the other ship, (HMS Nottingham), the motion had been of a mild
nature, and, in this case, a crossover comparison had been achieved. The symptomatology data showed that the number of subjects who suffered from severe
symptoms of motion sickness was too small to permit statistical analysis according
to the degree of severity (i.e., absent, mild, moderate, or severe), so they classified
these data as being present or absent. The results showed that scopolamine was
generally more effective than cinnarizine in protecting subjects against the symptoms of seasickness. In mild sea conditions, cinnarizine was better tolerated than
scopolamine, having fewer side effects. In heavier sea states, however, the subjects
found the side effects of scopolamine relatively more acceptable. Overall, these
particular researchers recommended that scopolamine was preferable to cinnarizine
during heavy sea states and that cinnarizine was considered to be the drug of choice
during mild to moderate seas, unlike Doweck et al. in the previous paragraph.
Wood and Graybiel (1972) have demonstrated that cinnarizine, which is a calcium antagonist similar to flunarizine, albeit less potent, increased the number of
rotations tolerated in a slow rotation room before the subject has developed motion
sickness. The protection was less than that provided by cyclizine, which they
considered to be the next most effective drug in the series. In that evaluation, they
demonstrated that the number of head movements tolerated was close to 30 more
for a 50 mg dose of cinnarizine, compared to a placebo, and close to 80 more for a
0.6 mg dose of scopolamine. Other calcium antagonists will be discussed later.
10.3
Intramuscular Injection of Medication
Graybiel and Lackner (1987) investigated the effectiveness of intramuscular
injections of scopolamine, promethazine, and dimenhydrinate in the treatment of
severe motion sickness during parabolic flight manoeuvres. Forty-seven subjects
took part in the study, each of whom has previously been exposed to parabolic
flight during which their susceptibility to motion sickness has been assessed. In the
earlier flights the provocative motion has been as passive as possible. This was not
only achieved by strapping the subjects in their seats as usual, but also by adding a
neck collar to minimise extraneous head movements. In one such flight the subject
was blindfolded, but not in the other. In later preliminary flights, either these
conditions were repeated to evaluate changes in response over time, or the subject
was allowed free head movement to assess the effect of this additional stimulus on
the motion sickness response.
In this investigation, 40 parabolic flight manoeuvres were carried out in a
modified KC-135 aircraft providing alternating exposures to zero G in free fall and
1.8–2.0 G, each lasting some 20–25 s. Motion sickness has been rated according to
the scoring system reported by Miller and Graybiel (1970a, b). Three different
intramuscular anti-motion sickness medications were used, namely, 50 mg of
dimenhydrinate, 0.43 or 0.5 mg dosages of scopolamine (these data were subsequently pooled because of the similarity of the dosages), and 25 and 50 mg dosages
10.3
Intramuscular Injection of Medication
201
of promethazine. They found that the majority of subjects benefited from injections
of either 50 mg of promethazine or 0.5 mg of scopolamine. Subjects who were
experiencing nausea and vomiting usually felt better within 10 min and this
improvement continued throughout the period of exposure to provocative motion.
This has not been the case, however, for subjects who were given injections of
50 mg of dimenhydrinate or 25 mg of promethazine.
Graybiel and Lackner (1987) concluded that these results suggested that
anti-motion sickness intramuscular drug injections might help to reduce certain
features of space motion sickness. In particular, they opined that subjects who
experienced a loss of performance might then feel capable of returning to their
specified tasks. In addition, they made the important point that these anti-motion
sickness medications which were found to be effective, namely, promethazine and
scopolamine, did not prevent the users from adapting to the provocative motion
environment, thereby providing a double benefit. However, there seem to be other
views on this subject, so that particular matter perhaps requires further
consideration.
In view of the fact that NASA uses intramuscular (I.M.) promethazine to treat
space motion sickness, Cowings et al. (2000) investigated the effects of promethazine on human performance, mood states and motion sickness. There have been
12 men in the study, mean age 36 ± 3.1 years. Each subject received one day of
drug free training in the tasks to be used and three days of treatment conditions that
consisted of an injection of one of the following: 25 mg of promethazine; 50 mg of
promethazine; or sterile saline. During the 3 treatment conditions, the subjects were
given 12 performance tasks and carried out 4 trials on each task. The subjects had
also undergone a motion sickness test in a rotating chair.
These workers found that a subject’s performance was significantly degraded
compared with a placebo in 5 out of 12 tasks with the 25 mg I.M. dose of
promethazine and on 8 out of 12 tasks with the higher 50 mg I.M. dose. Those
performance tasks that have been significantly degraded were as follows: choice
reaction time, code substitution, spatial transformation, non-preferred hand tapping,
two-finger tapping, air combat manoeuvering, critical tracking and the
symptom-monitoring device. Tolerance to motion sickness was significantly higher
with 25 mg of I.M. promethazine, whereas the 50 mg I.M. dose has not been as
effective. Although the increase in motion tolerance observed was statistically
significant, these workers noted that the degree of protection from symptoms was
relatively minor and none of the subjects reported being asymptomatic after
treatment. These results led Cowings et al. to pose the question: “…is the degree of
protection from symptoms [of motion sickness] achieved with promethazine
‘worth’ the pervasive and long-lasting decrements in performance observed?” This
is an interesting observation that is worthy of further consideration.
Brand (1970) has reported that studies of motion sickness in life rafts at sea have
indicated that a dose of 0.2 mg of scopolamine given intramuscularly can be
expected to control nausea and vomiting after they have developed. Side effects
were not very severe and the subject remained alert and cooperative. There was,
however, a higher incidence of dryness in the mouth in the scopolamine group
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compared with placebo apparently, however that was not found to be statistically
significant. Brand has suggested that the intramuscular route may present a useful
means of protecting subjects in circumstances where the oral route is not suitable
and the maintenance of alertness is important. I should stress, however, that this
combination of benefits lends itself to the treatment of those who are survivors at
sea; it is, nevertheless, a very interesting observation that requires further investigation in this situation.
Wood et al. (1990) investigated the therapeutic effects of intramuscular injections of certain anti-motion sickness drugs on some symptoms of motion sickness,
other than nausea and vomiting. The secondary symptoms which they have chosen
were based on a report by Graybiel et al. (1977) and included slowing of brain
waves, loss of performance, inhibition of gastric motility, and the sopite (sleepiness) syndrome.
Forty volunteers, 34 male and six female, aged between 18 and 29 years took
part in the study. It was divided into 5 separate investigations, in which 8 different
subjects were tested once each week, 2 of these investigations involved brain wave
recordings and 3, gastric emptying. Provocative stimulation was induced by active
head movements during rotation in a Contraves-Goerz chair with headrests forward,
back, and each side. The chair speed was computer-controlled to provide incremental increases according to the “step-test programme” (Graybiel and Knepton
1977; Oosterveld et al. 1972). The subjects were stimulated up to the M-III
end-point, short of nausea and vomiting on the Graybiel Motion Sickness Symptom
Scale (Table 6.1 in Chap. 6) In this programme, intramuscular injections of the
following anti-motion sickness drugs were evaluated: a 50 mg dose of dimenhydrinate; 25 mg of ephedrine; 0.1, 0.2 and 0.3 mg of scopolamine; 250 mg of caffeine; 5 mg of metoclopramide; 1 mg of glucagon and a placebo.
The Cornell Medical Index (Brodman et al. 1949) item questionnaire was then
administered to the subjects just before and just after rotation, in order to record the
side effects of the medications. The subjects’ brain waves were recorded on a Grass
Model 6 Electroencephalograph device before, immediately after, and at one and
two hours after reaching the MIII level of motion sickness. Gastric emptying was
studied after the subject had been given an oral dose of 1 Mci Technetium 99 m
DTPA in 10 oz isotonic saline. After rotation, it was found that increases in
dizziness and drowsiness over the pre-test levels were found with the placebo.
These were reduced when a dose of 50 mg of dimenhydrinate had been given at
the end of rotation. However, 25 mg of ephedrine only reduced dizziness and
drowsiness below the placebo level, but not to the level noted before rotation. All of
the intramuscular doses of scopolamine increased the side effects from a dose of
0.1 mg, which was just above the placebo level, to the higher doses that resulted in
a significant increase. The EEG recordings showed a slowing of alpha waves, with
some theta and delta waves from the frontal areas at the one and two hour points
following rotation. Slowing of cerebral activity was seen in 27 records after 25 mg
of ephedrine, and in three of six records with 50 mg of dimenhydrinate, whereas,
10.3
Intramuscular Injection of Medication
203
0.3 mg of scopolamine had an additive effect, producing slowing in seven out of
eight electroencephalographic recordings. Alterations in subject performance on the
pursuit meter, previously described, were shown to be correlated with these brain
wave changes (Wood et al. 1985). Gastric emptying was restored by
metoclopramide.
Wood et al. reported that ephedrine was effective in reducing some of the
secondary effects of motion sickness. Scopolamine was, as had been predicted,
effective in preventing nausea and vomiting, but it has not, however, been found to
reduce the secondary effects. On the contrary, scopolamine seemed to add to the
secondary effects. This led the authors to speculate that since the amphetamine
drugs relieved secondary symptoms, the norepinephrine-sensitive neurons were
inhibited by vestibular stimulation and perhaps also indirectly inhibited by
scopolamine. Wood et al. stated that scopolamine was the most effective drug for
the control of nausea and vomiting, and amphetamine was effective in managing the
secondary responses. They concluded, therefore, that the Scop/Dex combination
was the best choice of medication for preventing and treating motion sickness;
however, as we have already seen, intranasal scopolamine may alter this.
10.4
Dextroamphetamine Sulphate (Dexedrine®)
Dextroamphetamine (or dexamphetamine) stimulates the respiratory centre in the
medulla and shows other signs of stimulating the central nervous system. It has
been suggested that this action is due to stimulation of the cerebral cortex and
perhaps also the reticular activating system. This drug has greater action on the
central nervous system, and less peripheral action, than other adrenergic agonists.
However, it has been shown to protect against motion sickness when used alone
and also to act synergistically when combined with scopolamine or promethazine
(Wood 1990).
In various doses, these mixtures are considered to offer the most effective means
of pharmacological protection against motion sickness. Laboratory studies of the
scopolamine/dexamphetamine mixtures have been shown to improve tolerance of
provocative head movements. Dextroamphetamine also reduces the sleepiness and
decrement of performance produced by scopolamine. That is not the end of the
story, however. Dextroamphetamine is a controlled drug, and because of its
habituating properties, one cannot justify its routine use because of the possibility of
addiction. In this context, it would be advisable to replace dextroamphetamine with
ephedrine. That combination would be less effective but, nevertheless, laboratory
studies have shown that it is still better mixture than scopolamine or promethazine
alone. In addition, ephedrine has the advantage of not being a controlled substance
but, unfortunately, it is not free from undesirable side effects.
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10.5
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Pharmacological Treatment of Motion Sickness
Relative Effectiveness of Common Anti-motion
Sickness Drugs
Wood and Graybiel (1972) have reported on a series of anti-motion sickness drug
evaluations that began in 1963. This research programme included controlled
laboratory experiments in a slow rotation room, followed by evaluations of the
drugs in real-world settings both at sea and during acrobatic studies in flight. They
used a double-blind, placebo controlled technique and the combination of 0.6 mg of
Fig. 10.1 Relative effectiveness of certain drugs tested against motion sickness arranged in order
of effectiveness, including usually recommended doses, increased doses and combinations of
drugs
10.5
Relative Effectiveness of Common Anti-motion Sickness Drugs
205
scopolamine together with 10 mg of amphetamine was used as a standard for
comparison in all of these studies. The relative protection of the drugs tested is
shown in Fig. 10.1, in which they have been arranged in order of the effectiveness
of the usual recommended dose, together with increased doses and combinations of
medications. They concluded that scopolamine was the most effective drug in these
studies. They also noted that a dose of 0.6 mg of scopolamine seemed to be optimal
because doubling the dose to 1.2 mg only increased the effectiveness of the drug
slightly, whereas the unwanted effects of drowsiness and dry mouth rose to 76% of
subjects compared to 30% for the smaller dose. However, when the dose was
halved to 0.3 mg, the effectiveness had been reduced. On reflection, perhaps the
most remarkable feature of the drugs described in Fig. 10.1, is that some 40 years
later, we were still using most of these same drugs.
10.6
Other Anti-motion Sickness Drugs
Over the years many other drugs have been used to prevent motion sickness. For
example, Reason and Brand (1975), have listed opium, cocaine, strychnine, creosote, quinine, nitrous oxide, amyl nitrate, hydrocyanic acid, nitroglycerine, warm
salt water, coffee, tea, or alcohol. Most of them do not work, other than perhaps as
placebos, and many of them produce side effects that are totally unacceptable,
particularly for people carrying out skilled and potentially dangerous tasks. Many
other drugs have also being evaluated, e.g. phenytoin (Woodard et al. 1993).
Phenytoin (Dilantin®): This is an antiseizure drug that has been studied extensively in both laboratory and clinical settings. It acts diffusely upon the central
nervous system to stabilise neuronal membranes, but does not cause general
depression of the central nervous system. Following oral ingestion, the drug is
absorbed slowly; sometimes this is variable and may not be complete. It has been
reported that the peak plasma concentration of phenytoin following ingestion of a
single dose may occur as early as 3 h or as late as 12 h. It is, however, distributed
rapidly throughout all tissues after it has been absorbed (Smith et al. 1988).
Chelen et al. (1990) have carried out a placebo-controlled double-blind crossover pilot study of phenytoin to evaluate its ability to reduce motion sickness
induced by cross-coupled (Coriolos) stimulation in human subjects. They pointed
out that Smith et al. have demonstrated that phenytoin binds with active sodium
channels and perhaps with calcium channels also, thereby delaying their return from
the inactivated, unstable state and reducing the influx of sodium. In this experiment,
active head movements have been made every ten seconds as the subjects rotated in
the yaw axis, blindfolded, at constant rates of 14, 16, 18, 20, or 22 rpm. The head
movements were made throughout the full range, in the directions right/up, left/up,
down/up. Symptoms of motion sickness were recorded at 30-s intervals to the point
of emesis, or until the subjects aborted the run. In addition, the following physiological responses were also recorded: respiratory rate and volume, electroencephalogram, electrocardiogram, peripheral pulse volume, blood pressure,
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Pharmacological Treatment of Motion Sickness
electronystagmogram, electrogastrogram, bowel sounds, peripheral skin temperature and conductance.
In this study, Chelen et al. obtained a mean increase in subject tolerance to
cross-coupled (Coriolis) stimulation from 4.87 min (S.D. = 5.55) to 46.87 min (S.
D. = 32.6). They reported that this offered a greater than four-fold protection
against motion sickness over any single agent then available and more that twice the
effectiveness of scopolamine/Dexedrine combined; a mixture which has commonly
been reported as providing the greatest amelioration of symptoms. In addition, there
were no reports of the usual unpleasant side effects that are associated with
scopolamine, namely blurred vision, dryness of the mouth, dizziness, or sleepiness.
These researchers proposed to expand this evaluation with a greater number of
subjects in order to obtain additional dose-response data. This would be most
valuable, particularly in view of the reported variability in the rate of absorption of
phenytoin.
Woodard et al. (1993) have pointed out that seasickness is the most common
form of motion sickness; an observation made previously (Reason and Brand
1975). They stressed that this debility is a significant operational problem during
the retrieval of the Space Shuttle solid-fueled rocket booster. They also referred to
results from others (Chelen et al. 1990) that have indicated that phenytoin provided
protection against motion sickness that had been induced by cross-coupled
(Coriolis) stimulation. In their study they used 15 paid volunteers, aged 21–
51 years, who were crewmembers and divers working on solid-fueled rocket
booster recovery ships. Using a repeated-measures experimental design, Woodard
et al. exposed their subjects to 15° off-vertical rotation at 20 rpm counter-clockwise
and sea motion providing at least 3-foot waves, after the administration of
phenytoin or placebo. The subjects were given a loading dose of 500 to 1200 mg of
phenytoin that had been split into four portions, at 1000, 1400, 1800 h and finally
0600 h next morning. Subsequently, these subjects were then given a maintenance
dose of the drug that ranged from 100 to 200 mg every 24 h, based on the serum
half-life and volume distribution of the medication in each subject. They proceeded
by adjusting the dosage of the drug in order to obtain a blood level of >9–12 mg/
mL of the highest dose that has been free of side effects.
They found that phenytoin appeared to increase the duration of exposure to
off-axis provocative stimulation and that phenytoin blood levels of at least 9 µg/mL
were protective against motion sickness at sea. There was no change in the susceptibility of divers to nitrogen narcosis during chamber tests at 460 kPa while
performing two-digit and one-digit multiplication tests. Phenytoin has been
administered to the subjects before carrying out critical and hazardous tasks during
their training and also during actual recovery of rocket boosters. Their supervisors
did not notice any apparent degradation in the performance of these subjects, while
carrying out these particular tasks. Woodard et al. concluded, therefore, that
phenytoin has been effective in protecting crewmembers against motion sickness
while carrying out these recovery tasks.
Stern et al. (1994) tested the prophylactic effects of a single low dose of
phenytoin on motion sickness induced by illusory motion in an optokinetic drum.
10.6
Other Anti-motion Sickness Drugs
207
This double-blind study included 35 male college students who have previously
shown susceptibility to vection-induced motion sickness. Nineteen of these fasted
male subjects were given a 200-mg tablet of phenytoin, and 16 have been given a
placebo. The subjects were seated in an optokinetic drum, which was stationary for
8 min and then rotated at 10 rpm for a total of 16 min, or before then if the
symptoms of motion sickness became too uncomfortable. Subjects reported their
responses to this provocative stimulus every 2 min. Electrogastrograms (EGGs)
were recorded by placing two silver-silver chloride cutaneous electrodes on the
upper abdominal wall. The active electrode was placed approximately 4 cm from
the umbilicus, toward the head, and 3 cm to the left. The reference electrode was
placed between the umbilicus and the xiphoid process, 5 cm to the right of the
midline. EGG recordings were made before subjects had been given a drug, 4 h
after ingestion of the selected drug, before the start of rotation of the optokinetic
drum, and while the drum was rotating.
Although the subjects who had been given phenytoin had a lower mean subjective symptom score than the placebo group (5.8 vs. 7.1), the difference was not
statistically significant. However, 6 of the 16 subjects who had been given the
placebo aborted the test run in the optokinetic drum because of the severity of their
motion sickness, compared with 2 of the 19 subjects who had been given phenytoin. The group receiving phenytoin did not show any increase in gastric tachyarrhythmia during provocative illusory motion whereas this response, which has
normally been associated with nausea, was seen to be double for the placebo
group. Stern et al. concluded that this single low dose of phenytoin had significantly
reduced the intensity of the motion sickness effects of provocative motion.
Metoclopramide (Reglan®): Metoclopramide is a dopamine antagonist that also
blocks 5-HT3 (serotonin) receptors. It is an effective antiemetic agent that enhances
gastric emptying and prevents emesis induced by cancer chemotherapy. Kohl
(1987) elected to investigate its potential effectiveness in the prevention of motion
sickness. A total of 36 subjects have been divided into 3 groups. The first group
consisted of 11 subjects who had vomited during their only previous exposure to
parabolic flight. They were given an oral dose of 10 mg of metoclopramide during
this study. The 10 subjects in the second group had no previous experience with
parabolic flight, and were given a dose of 20 mg of the drug. The remaining 15
subjects were also given a 20 mg dose, but they were exposed to cross-coupled
(Coriolis) stimulation by means of active head movements on a rotating chair, using
a Staircase Profile test. The medication has been administered 75 min before
exposure to provocative motion. The aim of the investigation was to evaluate the
drug’s ability to prevent emesis or Nausea II (Table 6.1 in Chap. 6), respectively.
However, Kohl was unable to demonstrate any significant protective effects of
metoclopramide on motion sickness induced by these forms of provocative motion.
Cavinton: Matsnev and Bodo (1984) observed that despite the fact that the neural
mismatch hypothesis was still generally accepted as the best explanation of the
mechanisms of the space adaptation syndrome to date, however, one could not
exclude the contribution made by cephalad fluid shifts. For this reason, they
decided to investigate the effectiveness of cavinton as an anti-motion sickness drug.
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Pharmacological Treatment of Motion Sickness
The precursor of cavinton is vincamine, which is similar to reserpine, and is
modified to produce cavinton’s selective effect on the cerebral circulation.
Experiments have shown that it causes an increase in total blood flow and decreases
vascular resistance. In terms of cerebral blood flow, this drug shows its greatest
effect in the cortical layer of the cerebrum, the thalamus and the hypothalamus. The
effects on cerebral metabolism cause greater resistance to hemodynamic shifts.
Matsnev and Bodo have provided a schematic model of the extensive action of this
drug.
They compared a single dose of cavinton (10 mg) with 25 mg of Stugeron®
(cinnarizine) and 1 mg of scopolamine in protecting 20 healthy volunteers against
the effects of cross-coupled (Coriolis) stimulation. However, their results showed
that in the single dose regimen that had been used in this particular experiment
cavinton, unlike the other more well-known anti-motion sickness drugs, offered no
more protection than did the placebo. Matsnev and Bodo also investigated the
effectiveness of the drug on a prolonged basis using 30 healthy volunteers. They
concluded that the administration of cavinton at a dose of 10 mg, three times daily,
for 7 days did reduce the vestibulo-autonomic and somatic responses related to
motion sickness; in addition, there was no measurable degradation of mental performance. In addition, this regimen helped to maintain the subjects’ leg muscle tone
during head tilting. There have been no reported comparisons with other recognised
anti-motion sickness drugs over a 7-day period.
Other Sympathomimetic Drugs: Kohl et al. (1986) have pointed out that the
sympathomimetic drugs dextroamphetamine and ephedrine are commonly used to
counteract the sedative effects of commonly used anti-motion sickness drugs such
as scopolamine and promethazine. However, as already reported, these sympathomimetic drugs have protective properties against provocative motion in their own
right. In addition, it has been shown that their combination with anticholinergic
drugs or antihistamines resulted in a synergistic increase in the overall effectiveness
of the drug combinations. This led others to postulate that noradrenergic inhibitory
mechanisms were involved in the amelioration of motion sickness.
It has also been reported that arousal in general can have protective effects. For
example, Kohl et al. quoted an astronaut report to the effect that space motion
sickness did not seem to occur during severe emotional stress and Russian statements that nonspecific arousal also seemed to provide protection. They have
pointed out that the arousal systems are located in the locus ceruleus of the brain
with noradrenergic projections consistent with the activating effects of sympathomimetic drugs. This question of the protection afforded by certain types of arousal
that focuses attention fits well with Schwab’s (1954) observations already discussed
in the section dealing with the “Effect of Arousal on the Incidence of Motion
Sickness.”
In view of these considerations, Kohl et al. evaluated the anti-motion sickness
properties of five new sympathomimetic drugs and attempted to define the part
played by arousal in a person’s susceptibility to provocative motion. The study was
carried out with 20 male and 7 female subjects. Each of the 5 different oral drugs,
namely, 20 mg of methamphetamine, 25 mg of phenmetrazine, 37.5 mg of
10.6
Other Anti-motion Sickness Drugs
209
phentermine, 20 mg of methylphenidate, 75 mg of pemoline, or a placebo was
administered to 18 of the subjects prior to inducing provocative stimulation by
means of active head movements during bodily rotation, using a Staircase Profile
Test procedure. The remaining 9 subjects were given a placebo in all of the
experiments.
They found that all of the drugs increased resistance to cross-coupled (Coriolis)
provocative stimulation by some 80–120%. They also noted that methylphenidate
and pemoline showed fewer side effects. In view of these findings and the relative
inefficacy of most anticholinergic and antihistaminergic drugs tested to date, Kohl
and his colleagues suggested that sympathomimetic drugs, or a generalised state of
arousal, could inhibit the development of motion sickness.
In 1974, I made use of arousal-attention mechanisms in the development of my
cognitive-behavioural training programme and later, also used these in the management of other stressors. In 1989, my colleagues and I tested the use of focus of
attention in the counselling component of the cognitive-behavioural anti-motion
sickness training programme to suppress the unpleasant effects of provocative
motion, as readers will note later in Chap. 13, when I discuss this programme in
some detail.
Ginger Root: Stott et al. (1984) conducted a double-blind laboratory trial involving
16 male subjects, aged 16–44 years, to evaluate the effectiveness of powdered
ginger root in comparison with scopolamine (hyoscine hydrobromide), cinnarizine,
and a placebo. They measured increased tolerance to motion sickness induced by
cross-coupled (Coriolis) stimulation produced by active head movements while the
subjects have been seated on a rotating platform.
The subjects were given one of the following compounds 2 h before the start of
each trial: 0.6 mg scopolamine, 15 mg cinnarizine, 1 g powdered ginger root, or
1 g lactose (placebo). Each substance was contained in two identical gelatin capsules so that neither the subject nor the experimenter was aware of which substance
has been given and administration was randomised by means of non-repeating Latin
squares. In addition, each subject has been tested at the same time of the day, at
intervals of seven days, over a period of four weeks.
The results showed that scopolamine produced the greatest increase in subject
tolerance to motion sickness induced by cross-coupled (Coriolis) stimulation.
Cinnarizine was more effective than both of the others, and there was no significant
difference between ginger root and placebo. As Stott et al. have concluded: “The
principal finding from this experiment was the absence of any significant therapeutic, or other effect, of powdered ginger root.” This result is in keeping with that
found by Wood and Graybiel (1972), as shown in Fig. 10.1.
Calcium Antagonists: In a letter to the editor of The Lancet, Marley and Joy
(1987) reported their experience with a 39-year-old man who suffered severe
motion sickness throughout his life. His occupation needed him to cross the English
Channel often. As a hypertensive, he was taking part in a clinical trial in which he
had been randomised to atenolol (Tenormin®) and nifedipine (Adalat®,
Procardia®). During this treatment, he reported spontaneously that his susceptibility
to travel sickness had apparently resolved without his taking any anti-motion
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sickness medication. He also noticed that there had been no improvement in his
seasickness with atenolol alone. He was then given 20 mg of sustained-release
nifedipine, to be taken twice daily in an open fashion for subsequent channel
crossings and every time the journey was trouble-free.
Calcium ions are present in the endolymph. In response to movement of the
endolymph there is a calcium ion flux into the cells of the crista ampullaris, triggering action potentials, which travel centrally. Nifedipine is a calcium channel
blocker, and Marley and Joy have suggested that this anti-motion sickness protective effect may be caused by the action of nifedipine antagonising the influx of
calcium ions into the vestibular cells.
Flunarizine is a proven calcium channel blocker (Van Neuten 1973). It is a
calcium antagonist that has been shown to exert a powerful, peripherally acting
suppressant action on the labyrinth of the inner ear. It has been proven to be
clinically useful in controlling chronic vertigo and has an application in the prevention of motion sickness. However, flunarizine did not seem to produce major
central depressive side effects associated with the anti-motion sickness medications
in common use, namely, the antihistamines and the anticholinergic drugs, even
though it also has antihistamine properties. In a double-blind crossover trial
involving 10 male subjects, aged 22–37 years, Lee et al. (1986) compared the
electronystagmic responses to rotational motion in a darkened disorientation trainer,
following the ingestion of one of these drugs on each test day: 10 or 30 mg of
flunarizine, 5 mg of prochlorperazine maleate, or a placebo.
Their study has shown that flunarizine in both the 10 and 30-mg dose has a
significant depressant action on the vestibular apparatus. They found a high correlation between the reduction of the duration of nystagmus and the reduction of
peak velocity of the slow phase of nystagmus. Since the latter has indicated
peripheral vestibular sensitivity, they deduced that the suppression of nystagmus
induced by flunarizine was the result of a peripheral, rather than central, action.
They pointed out that this conclusion agreed with the results of torsion swing tests
that were carried out by Oosterveld (1974) and caloric tests that have been performed by Scherer et al. (1978). These workers have both demonstrated a reduction
in the velocity of the slow phase of nystagmus with flunarizine.
Wovters et al. (1983) reported on the results of administering flunarizine during
double-blind, controlled clinical trials on patients with chronic labyrinthine vertigo.
These studies have shown a reduction in the frequency duration, and severity of
vertigo, together with decreased labyrinthine excitability as shown by electronystagmography. The main side effect of the ingestion of flunarizine has been
drowsiness, but this occurred in less than 5% of the patients. Although flunarizine
has not been evaluated in specific tests involving provocative motion, nevertheless
Lee et al. (1986) believed that their experimental results suggested that flunarizine
has promise as an anti-motion sickness drug.
10.7
10.7
Theoretical Considerations
211
Theoretical Considerations
As I have stated previously, this review is not intended to be a comprehensive
evaluation of drug therapy in the prevention of motion sickness. For one thing,
many experts, such as Tyler and Bard (1949), Chinn and Smith (1953), Wood et al.
(1965), Brand and Perry (1966) and Wood (1990) have already published such
comprehensive documents. Rather, it sets out to explore briefly the limitations of
this approach, particularly in terms of the skilled operator (not the passenger).
Undoubtedly there is a significant place for the use of anti-motion sickness medication, it is not the only effective approach. Perhaps the best solution to the management of motion sickness, particularly for passengers lies in finding the best
protection for a given set of people based on what they will be doing when the need
arises.
Glaser and Hervey had reported an interesting observation in 1952 concerning
symptoms reported by subjects during experimental studies of anti-motion sickness
drugs. In that study they found that the subjective symptoms of headache,
drowsiness and giddiness were nearly as frequent after ingesting the placebo
(lactose) as they have been after any of the drugs or combinations of drugs used in
the study. These were 1 mg of l-hyoscine hydrobromide (scopolamine), 35 mg of
promethazine hydrochloride (Phenergan®), 1 mg of hyoscine hydrobromide with
25 mg of promethazine hydrochloride, 0.65 mg of hyoscine hydrobromide with
15 mg of promethazine hydrochloride and 0.65 mg of hyoscine hydrobromide with
both 15 mg of promethazine hydrochloride and 50 mg of mannitol hexanitrate.
They found that excitement was uncommon after any treatment. They also noted
that light-headedness, sleepiness and mild gastro-intestinal disturbances occurring a
few hours after the provocative motion exposures were reported as frequently after
ingesting the placebo (lactose) as they had been after any of the active drugs. These
observations complicate the interpretation of experimental results because of the
difficulty of discriminating between symptoms due to motion effects, the unwanted
effects of active drugs and individual responses to questionnaires even after the
ingestion of placebos—due to suggestion. On the subject of placebos, Tyler (1946)
has carried out an interesting controlled study at sea to investigate the influence of a
placebo on the incidence and severity motion sickness. In a series of four experiments, 563 subjects were loaded on barges from the beach, taken out to sea where
they underwent manoeuvres and then returned to the beach to disembark.
A comparison of the results between untreated controls and placebo controls is
shown in Table 10.1. Those in the placebo group had not been aware that their
“medication” was a placebo. In summary, Tyler found that there was no significant
difference between these two groups.
One must also bear in mind that the protective effects found in laboratory
studies, such as those involving head movement in a provocative motion environment, are not always confirmed in the real world. For example, Tokola et al.
(1984) found that adding ephedrine did not significantly increase the protection
afforded by scopolamine alone during a trial at sea. As Oosterveld (1991) has
212
10
Pharmacological Treatment of Motion Sickness
Table 10.1 Effect of a placebo on incidence of seasickness
Experimental
groups
No. of
men
No. M.
S.
Experiment 1
Untreated
68
16
controls
Placebo
54
9
controls
Experiment 2
Untreated
107
22
controls
Placebo
72
16
controls
Experiment 3
Untreated
67
15
Placebo
70
12
Experiment 4
Untreated
61
14
Placebo
64
12
Summary of the four experiments
Untreated
303
67
Placebo
260
49
MS moderately sick; SS severely sick; IC
No. S.
S.
No. I.
C.
Total
sick
Percent
S.S. (%)
Percent
sick (%)
6
0
22
9
32
5
0
14
9
26
10
0
32
9
30
6
0
22
8
31
12
18
2
2
29
32
21
29
43
46
8
9
1
0
23
21
15
14
38
33
106
89
13
15
35
34
36
3
38
2
incapacitated
pointed out, although laboratory models are useful to some extent, one must always
remember that “the final proof must be sought under the conditions in which a drug
is expected to work.” I should add that the author is.
Cheung et al. (1992) have developed an animal model for anti-motion sickness
drugs using the squirrel monkey (Saimiri sciureus). As they pointed out, earlier
attempts using dogs and cats failed to provide a useful model. Using the squirrel
monkey, Cheung et al. were able to define the therapeutic dose range of those
anti-motion sickness drugs that have already been shown to protect human subjects.
They concluded that their approach had the great advantage of allowing a large
number of potentially useful drugs to be tested across a wide range of dosages.
The pharmacological approach to the treatment of motion sickness introduces
many problems. The drug actions are variable both in terms of individual responses
and the effects of an operational situation on these responses. Some of the potential
side effects are not acceptable when the user is in control of sophisticated or
potentially hazardous equipment, or making complex operational command and
control decisions.
Ships’ crewmembers who are performing skilled mental and physical tasks on
board ship should not be given medications that degrade performance. Personnel
who are not at their best mentally cannot reliably and correctly make command and
control decisions. Nor should individuals whose comprehension and decisions are
10.7
Theoretical Considerations
213
clouded by side effects that degrade performance be carrying out complex or
potentially dangerous physical tasks. With modern sophisticated ships and equipment that depend upon fewer operators, maximal crew effectiveness is critical. This
problem is likely to get worse if, as anticipated, future ships are designed to
accommodate smaller crews.
Flight crews also perform both skilled and potentially dangerous tasks most of
their working lives, and any decrement of performance brought about by medication can be very serious. The use of an anti-motion sickness drug should be
restricted to those situations where a trainee is flying dual and therefore not in sole
charge of the aircraft, nor responsible for a critical operating task in the air. Nor
should physicians prescribe anti-motion sickness medication to flight crews for long
periods, lest they become dependent upon the drug. Many individuals who have
grown accustomed to the protection afforded by anti-motion sickness medications
are known to become apprehensive about flying without them. In terms of civil
aviation, the application of any pilot for medical certification must be deferred and
sent for FAA approval if he or she is on continuous treatment with tranquilizers,
motion sickness, sedating antihistaminic, or sedative drugs, among others that are
not usually associated with motion sickness (Silberman 2003). Although dexamphetamine was not specifically mentioned in that paper, Silberman stated that
stimulants are usually not permitted for pilots.
For the protection of passengers and those whose motion exposures are infrequent, or for survivors exposed to severe motion environments in an emergency,
such as in a life raft, the search for the most suitable medication and route of
introduction is a separate but critically important matter, which requires further
study.
In summary, the pharmacological approach to the treatment of motion sickness
is neither simple nor straightforward, as clearly stated by Charles Wood and his
colleagues, who are some of the foremost workers in that field.
In the words of Wood et al. (1985):
It is scientifically possible for a skilled flight surgeon to select antimotion sickness medications that would be acceptable for an operational situation. Knowledge of the medication
and its side effects at the effective dosage range would first be required. Then the response
of the individual to that dose of the drug in a nonoperational setting should be observed. In
addition, a thorough knowledge of the requirements of the operational duties is needed.
This information with the results presented here should permit the selection of anti-motion
sickness drug combinations and dosage levels that would be therapeutically effective and
produce no loss of operational proficiency.
There are many potentially serious implications contained in these comments.
A great deal of complex investigation is required to find medications that are both
safe and suitable for use in operational situations; much of this is not traightforward.
Individual responses to the actions of drugs are not always predictable nor are they
reproducible from exposure to exposure. During critical operational scenarios at
sea, in the air, and on the ground, other avenues should be thoroughly investigated
in order to protect individuals from the deleterious effects of motion sickness before
resorting to potentially hazardous medications.
214
10.8
10
Pharmacological Treatment of Motion Sickness
Summary
• The use of various drugs has been the most common treatment for motion
sickness symptoms, but there is concern over both the effectiveness and the side
effects of these drugs, that might degrade performance.
• Drugs have different lead times before becoming effective; they also have different durations of action. The choice of drug, or mixture of drugs, should reflect
the underlying situational requirement for the medication.
• The effects of combinations of anti-motion sickness drugs on human performance may be measured through tests of cognitive and psychomotor skills.
• The most effective combination of drugs for treatment and prevention of primary and secondary symptoms of motion sickness are scopolamine and
amphetamine.
• Since amphetamine is a controlled substance it is not recommended and
scopolamine or promethazine are the drugs of choice.
• In view of the problems associated with anti-motion sickness medications,
serious consideration should be given to a non-pharmacological approach for
managing motion sickness.
References
Attias J, Gordon C, Ribak J, Binah O, Rolnick A (1987) Efficacy of transdermal scopolamine
against seasickness: a 3-day study at sea. Aviat Space Environ Med 58:60–62
Brand JJ (1970) A survey of recent motion sickness research. J R Nav Med Serv 56:204–207
Brand JJ, Perry WLM (1966) Drugs used in motion sickness. A critical review of the methods
available for the study of drugs of potential value in its treatment and of the information which
has been derived by these methods. Pharmacol Rev 18(1):895–924
Brand JJ, Colquhoun WF, Gould AF, Perry WLM (1965) A study of the relative potencies of
l-hyoscine and cyclizine in preventing motion sickness, in preventing side effects, and in
affecting mental performance. R.N.P. 66/1068, S.S. 155. Medical Research Council, Royal
Naval Personnel Research Committee
Brazell C, Preston GC, Ward C, Lines CR, Traub M (1989) The scopolamine model of dementia:
chronic transdermal administration. J Psychopharmacol 3:76–82
Brodman K, Erdman AJ Jr, Wolff HG (1949) Cornell medical index health questionnaire—
manual. Cornell University Medical College, New York
Chelen W, Kabrisky M, Hatsell C, Morales R, Fix E, Scott M (1990) Use of phenytoin in the
prevention of motion sickness. Aviat Space Environ Med 61:1022–1025
Cheung BSK, Money KE, Kohl RL, Kinter LB (1992) Investigation of anti-motion sickness drugs
in the squirrel monkey. J Clin Pharmacol 32(2):163–175
Chinn HI, Smith PK (1953) Motion sickness. Pharmacol Rev 7:33
Cowings PS, Toscano WB, DeRoshia C, Miller NE (2000) Promethazine as a motion sickness
treatment: impact of human performance and mood states. Aviat Space Environ Med 71:1013–
1022
Doweck I, Gordon CR, Spitzer O, Melamed Y, Shupak A (1994) Effect of cinnarizine in the
prevention of seasickness. Aviat Space Environ Med 65:606–609
References
215
Estrada A, Le Duc PA, Curry IP, Phelps SE, Fuller DR (2007) Airsickness prevention in helicopter
passengers. Aerosp Med Assoc 78(4):408–413
Evans MA, Martz R, Rodda BE, Kilplinger GF, Forney RB (1973) Quantitative relationship
between blood alcohol concentration and psychomotor performance. Clin Pharmacol Ther
15:253–260
Fleishman E, Quaintance M (1984) Taxonomics of human performance. Wiley, New York
Glaser EM, Hervey GR (1952) Further experiments on the prevention of motion sickness. Lancet
490–492
Golding JF, Strong R, Pethybridge R (1988) Time course of oral Cinnarizine effects on task
performance. INM REPORT 18/88, Institute of Naval Medicine, Gosport, Hants, UK
Golding JF, Gosden E, Gerrell J (1991) Scopolamine blood levels following buccal versus
ingested tablets. Aviat Space Environ Med 62:521–526
Gordon C, Binah O, Attias J, Rolnick A (1986) Transdermal scopolamine: human performance
and side effects. Aviat Space Environ Med 57:236–240
Graybiel A, Knepton J (1977) Evaluation of a new antinauseant drug for the prevention of motion
sickness. Aviat Space Environ Med 48:867–871
Graybiel A, Lackner JR (1987) Treatment of severe motion sickness with antimotion sickness drug
injections. Aviat Space Environ Med 58:773–776
Graybiel A, Miller EF, Homick JL (1977) Human vestibular function. In: Johnston RS,
Dietlein LF (eds) Biomedical results from SkyLab. NASA SP-377, National Aeronautics and
Space Administration, Washington, D.C.
Hardman JG, Limbird LE, Molinoff PB, Ruddon RW (eds) (1996) Goodman and Gilman’s the
pharmacological basis of therapeutics, 9th edn. McGraw-Hill, New York
Holling HE, McArdle B, Trotter WR (1944) Prevention of seasickness by drugs. Lancet I:127–129
Jennings RT, Beck BG, Davis JR, Bagian JP (1993) Treatment efficacy of IM promethazine for
space motion sickness in first flight shuttle crewmembers. Aviat Space Environ Med 64:423
(Abstract #27)
Kennedy RS, Odenheimer RC, Baltzley DR, Dunlap WP, Wood CD (1990c) Differential effects of
scopolamine and amphetamine on microcomputer-based performance tests. Aviation, Space,
and Environmental Medicine 61: 615–621
Kennedy RS, Wood CD, Graybiel A, McDonough RB (1966) Side effects of some anti-motion
sickness drugs as measured by psychomotor test and questionnaires. Aerosp Med 37:408–411
Kohl RL (1987) Failure of metoclopramide to control emesis or nausea due to stressful angular or
linear acceleration. Aviat Space Environ Med 58:125–131
Kohl RL, Calkins DS, Mandell AJ (1986) Arousal and stability: the effects of five new
sympathomimetic drugs suggest a new principle for the prevention of space motion sickness.
Aviat Space Environ Med 57:137–143
Lawther A, Griffin MJ (1988) A survey of the occurrence of motion sickness amongst passengers
at sea. Aviat Space Environ Med 59:399–406
Lee JA, Watson LA, Boothby G (1986) Calcium antagonists in the prevention of motion sickness.
Aviat Space Environ Med 57:45
Lucot JB (1998) Pharmacology of motion sickness. J Vestib Res 8(1):61–66
Marley JE, Joy MD (1987) Alleviation of motion sickness by nifedipine. Lancet 2:1265
Matsnev EI, Bodo D (1984) Experimental assessment of selected antimotion drugs. Aviat Space
Environ Med 55(4):281–286
Miller EF, Graybiel A (1970a) A provocative test for grading susceptibility to motion sickness
yielding a single numerical score. Acta Otolaryngol 5(274)
Miller EF, Graybiel A (1970b) Motion sickness produced by head movement as a function of
rotational velocity. Aerosp Med 41:1180–1184
Nieuwenhuijsen JH (1958) Experimental investigations on seasickness. Ph.D. thesis, University of
Utrecht, The Netherlands
Norfleet WT, Degioanni JJ, Calkins DS, Reschke MF, Bungo MW, Kutyna FA, Homick JL (1992)
Treatment of motion sickness in parabolic flight with buccal scopolamine. Aviat Space Environ
Med 63:46–51
216
10
Pharmacological Treatment of Motion Sickness
Noy S, Shapiro S, Zilbiger A, Ribak J (1984) Transdermal therapeutic system scopolamine
(TTSS), dimenhydrinate, and placebo—a comparative study at sea. Aviat Space Environ Med
55:1051–1054
Oosterveld WJ (1974) Vestibular pharmacology of flunarizine compared to that of cinnarizine.
Oto-Rhino-Laryngologica 36:157–164
Oosterveld WJ (1991) Assessment of drug effectiveness. In: Motion sickness: significance in
aerospace operations and prophylaxis. Conference proceedings no 175, AGARD-LS-175,
North Atlantic Treaty Organization Advisory Group for Aerospace Research and
Development, Neuilly-sur-Seine, France, vol 10, pp 1–8
Oosterveld WJ, Graybiel A, Cramer DB (1972) Influence of vision on susceptibility to acute
motion sickness studied under quantifiable stimulus-response conditions. Aerosp Med 43
(9):1005–1007
Parrott AC (1989) Transdermal scopolamine: a review of its effect upon motion sickness,
psychological performance, and physiological functioning. Aviat Space Environ Med 60:1–9
Paul MA, MacLellan M, Gray G (2005) Motion sickness medications for aircrew: impact on
psychomotor performance. Aviat Space Environ Med 76:560–565
Payne RB, Moore EW, Bethurum JL (1952) The effects of certain motion sickness preventatives
upon psychological efficiency. USAF School of Aviation Medicine, No 21-32-019, Report 1
Payne RB, Osier DR, Tomlinson PAS (1953) The effects of certain motion sickness preventatives
upon navigator efficiency. USAF School of Aviation Medicine, No 21-1601-0004, Report 1
Physicians’ Desk Reference (2000) Montvale, NJ: medical economics company, 54th edn
Pingree BJW, Pethybridge RJ (1989) A double-blind placebo-controlled comparison of hyoscine
with early administered cinnarizine in increasing tolerance to a nauseogenic cross-coupled
motion challenge. Pharm Med 4:29–42
Pingree BJW, Pethybridge RJ (1994) A comparison of the efficacy of cinnarizine with
scopolamine in the treatment of seasickness. Aviat Space Environ Med 65:597–605
Putcha L, Berens KL, Marshburn TH, Ortega HJ, Billica RD (1999) Pharmaceutical use by U.S.
astronauts on space shuttle missions. Aviat Space Environ Med 70:705–708
Pyykko I, Padoan S, Schalen L, Lyttkens L, Magnusson M, Henriksson NG (1985) The effects of
TTS-scopolomine, dimenhydrinate, lidocaine, and tocainide on motion sickness, vertigo and
nystagmus. Aviat Space Environ Med 56:777–782
Reason JT, Brand JJ (1975) Motion sickness. Academic Press, New York
Regan EC, Ramsey AD (1996) The efficacy of hyoscine hydrobromide in reducing side-effects
induced during immersions in virtual reality. Aviat Space Environ Med 67:222–226
(Stuttgart)
Schmedtje JF Jr, Oman CM, Letz R, Baker EL (1988) Effects of scopolamine and dextroamphetamine on human performance. Aviat Space Environ Med 59:407–410
Schmitt MN, Shaw JE (1981) Comparison of transdermal and intravenous administration of
scopolamine. Clin Pharmacol Ther 29:282
Schwab RS (1954) The nonlabyrinthine causes of motion sickness. Int Rec Med Gen Pract Clin
167(12):631–637
Silberman WS (2003) Medications in civil airmen: what is acceptable and what is not. Aviat Space
Environ Med 74:85–86
Simmons RG, Phillips JB, Lojewski RA, Wang Z, Boyd JL, Putcha L (2010) The efficacy of
low-dose intranasal scopolamine for motion sickness. Aviat Space Environ Med 81(4):405–
412
Smith BH, Bogoch S, Dreyfus J (1988) The broad range of clinical use of phenytoin: biolectric
modulator. Dreyfus Medical Foundation, New York
Stern RM, Uijtdehaage SHJ, Muth ER, Koch KL (1994) Effect of Phenytoin on vection-induced
motion sickness and gastric myoelectric activity. Aviat Space Environ Med 65:518–521
Stott JRR (1991) Management of acute and chronic motion sickness. In: Motion sickness:
significance in aerospace operations and prophylaxis. AGARD Lecture series no 175,
AGARD-LS-175, North Atlantic Treaty Organization Advisory Group for Aerospace Research
and Development, Neuilly-sur-Seine, France, vol 11, pp 1–7
References
217
Stott JRR, Hubble MP, Spencer MB (1984) A double blind comparative trial of powdered ginger
root, hyoscine hydrobromide, and cinnarizine in the prophylaxis of motion sickness induced by
cross coupled stimulation. In: Motion sickness: mechanisms, prediction, prevention and
treatment. AGARD conference proceedings No 372 (AGARD-CP-372), North Atlantic Treaty
Organization Advisory Group for Aerospace Research and Development, Neuilly-sur-Seine,
France, vol 39, pp 1–5
Tokola O, Laitinen LA, Aho J, Gothoni G, Vapaatalo H (1984) Drug treatment of motion sickness:
scopolamine alone and combined with ephedrine in real and simulated situations. Aviat Space
Environ Med 55:636–641
Tyler DB (1946) Influence of placebo, body position and medication on motion sickness. Am J
Physiol 146:450–466
Tyler DB, Bard P (1949) Motion sickness. Physiol Rev 311–369
Uijtdehaage SHJ, Stern RM, Koch KL (1993) Effects of scopolamine on autonomic profiles
underlying motion sickness susceptibility. Aviat Space Environ Med 64:1–8
van Neuten JM, Janssen PAJ (1973) Comparative study of the effects of flunarizine and cinnarizine
on smooth muscles and cardiac tissues. Arch Int Pharmacodyn Ther 204:37–55
Wang ET, Zhou DR, He LH (1992) Histaminergic response to Coriolis stimulation: implication for
transdermal scopolamine therapy of motion sickness. Aviat Space Environ Med 63:579–582
Weerts AP, Pattyn N, Van de Heyning PH, Wuyts FL (2014) Evaluation of the effects of
anti-motion sickness drugs on subjective sleepiness and cognitive performance in healthy
males. J Psychopharmacol 28(7):656–664
Weinstein SE, Stern RM (1997) Comparison of marezine and Dramamine in preventing symptoms
of motion sickness. Aviat Space Environ Med 68:890–894
Wiker SF, Kennedy RS, McCauley ME, Pepper RL (1979) Susceptibility to seasickness: influence
of hull design and steaming direction. Aviat Space Environ Med 50:1046–1051
Wood CD (1990) Pharmacological countermeasures against motion sickness. In: Crampton GH
(ed) Motion and space sickness. CRC Press Inc., Boca Raton
Wood CD, Graybiel A (1972) Theory of antimotion sickness drug mechanisms. Aerosp Med 43
(3):249–252
Wood CD, Kennedy RS, Graybiel A (1965) Review of antimotion sickness drugs from 1954–
1964. Aerosp Med 1:1–4
Wood CD, Manno JE, Manno BR, Redetzki HM, Wood MJ, Mims ME (1985) Evaluation of
antimotion sickness drug side effects on performance. Aviat Space Environ Med 56:310–316
Wood CD, Manno JE, Manno BR, Odenheimer RC, Bairnsfather LE (1986) The effect of
antimotion sickness drugs on habituation to motion. Aviat Space Environ Med 57:539–542
Wood CD, Stewart JJ, Wood MJ, Manno JE, Manno BR, Mims ME (1990) Therapeutic effects of
antimotion sickness medications on the secondary symptoms of motion sickness. Aviat Space
Environ Med 61:157–161
Woodard D, Knox G, Myers KJ, Chelen W, Ferguson B (1993) Phenytoin as a countermeasure for
motion sickness in NASA maritime operations. Aviat Space Environ Med 64:363–366
Wovters L, Amery W, Towse G (1983) Flunarizine in the treatment of vertigo. J Laryngol Otol
97:697–704
Chapter 11
The Use of Non-pharmacological
Therapy
Abstract There are a number of non-pharmacological forms of therapy for
managing motion sickness. These have had varying degrees of success over the
years. The biggest problem I see in comparing the results of these various desensitising programmes is that all but mine excluded an undisclosed number of
potential candidates who showed less than desirable enthusiasm for continuing to
fly. Despite the fact that my cognitive-behavioural desensitisation training programme had no such pre-selection criteria, it was found to have the highest success
rate. Most of the other desensitisation training programmes involved biofeedback.
I do not support that approach because it relies on mental relaxation techniques to
control the individual’s physiological state, whereas I believe that the subject’s
mind should be both strongly focused and targeted elsewhere; that alone can protect
against provocative motion. In addition it is my strongly held opinion that it is
better to avoid the need to record physiological responses, for two reasons. First, it
seems to conflict with the idea that motion sickness is a normal protective response.
Second, military professionals and astronauts tend to be suspicious of physiological
recordings lest they have an adverse effect on their medical status.
In view of the potential problems associated with anti-motion sickness medications,
some form of behavioural desensitisation training has much to offer for preventing
or managing motion sickness, particularly for persons who are regularly exposed to
provocative motion environments. This form of management is particularly relevant
to an occupational situation, where the vast majority of these individuals are likely
to be carrying out some form of skilled or potentially hazardous tasks. It is this
group of people who can gain the greatest benefit from non-pharmacological procedures. It should be said, however, that passengers who experience less frequent
exposure to provocative motion have also benefited greatly from my
cognitive-behavioural anti-motion sickness training while travelling socially and
carrying out sporting activities. This particular technique will be reviewed in some
detail in Chap. 12.
A number of different forms of management have been developed in various
centres around the world to treat motion sickness without recourse to medication.
© Springer Nature Switzerland AG 2019
T. G. Dobie, Motion Sickness, Springer Series on Naval Architecture,
Marine Engineering, Shipbuilding and Shipping 6,
https://doi.org/10.1007/978-3-319-97493-4_11
219
220
11
The Use of Non-pharmacological Therapy
Table 11.1 Military desensitisation programmes
Program years
Totals
Successfully
desensitized
Successfully
desensitizeda
Total failure
Total success
a
Failed flight training
RAF
(Pre 74)
RAF
(74–80)
RAF
(81–83)
USAF
(79–85)
CF
(81–91)
USN
(75–78)
N = 50
76%
N = 46
67%
N = 32
72%
N = 34
62%
N = 22
54%
N=8
–
12%
15%
23%
–
14%
30%
16%
23%
86%
70%
84%
77%
for reasons other than motion sickness
22%
77%
–
62.5%
10%
2%
These fall into two broad categories of motion desensitisation, depending upon
whether they use some form of biofeedback or not. The overall available results of
these desensitisation programmes are summarised later in this chapter under
“Review of Military Desensitisation Programmes” and they are also tabulated in
Table 11.1.
11.1
RAF Desensitisation Programme
When I was assigned to HQ Flying Training Command in the Royal Air Force, it
became apparent that motion sickness was a serious problem that was causing the
loss of valuable pilot trainees. First, I looked at various screening questionnaires
and physical tests to see if I could identify volunteers likely to be susceptible to
airsickness. After collecting a large number of completed questionnaires at the
Selection Centre, I collected another like series from the same people who had been
selected and I rejected the selection system because I found that very few volunteers
had admitted their susceptibility to motion sickness in the first series at the Selection
Centre.
I then turned to the various ‘physical tests” that were in vogue at the time and
found that Lentz (1984) at Pensacola had reviewed the current tests and felt that all
of them had a very low correlation with the conditions in the real world.
So I decided to try a different new test from the Netherlands called cupulometry, but
as you also saw in Chap. 8, there was no significant correlation between the mean
value for the slope and threshold of the cupulograms and the subject’s: previous
flying experience; previous history of motion sickness; or subsequent susceptibility
to airsickness during training; so it failed to live up to what we had expected and
had to be removed from use. Since neither the screening questionnaires nor the
physical tests had been shown to be useful, I had no choice but to come up with a
new anti-motion sickness training programme to help. I am happy to say that after
delaying the decision for five years it was shown to have helped trainee fliers who
had been suffering from severe, and in many cases apparently intractable, airsickness (Dobie 1974). The only other treatment available at that time had been some
11.1
RAF Desensitisation Programme
221
form of anti-motion sickness medication. That form of management had been
restricted to dual-only sorties, however, because the side effects of these drugs had
been considered unacceptable, and potentially dangerous, when flying solo.
A considerable amount of expensive flight training time had been lost and in the
very worst cases of apparently intractable motion sickness, these flight trainees had
been grounded permanently. Many questions arose concerning the prevention and
treatment of airsickness, but at that time not many hard answers were available.
Early RAF Cognitive-Behavioural Approach: Flight trainees who were about to
be grounded permanently with the diagnosis “intractable airsickness” had been
placed on administrative hold while their future was being decided. This made them
available on a full-time basis for a last chance to recover and return to flight
training, if they could be helped to overcome their airsickness. The diagnosis:
“intractable airsickness,” had been made by local flight instructors, training staff,
and clinical physicians dealing with the particular trainee; I had not been involved
in that decision in any way.
Since there was no other avenue open to these trainees, I decided to try to
manage their problem in the hope that they could return to flight training successfully and eventually become useful, productive operational flight crew. This
meant devising a method of management, now known as cognitive-behavioural
desensitisation training, which did not involve medications.
My method of dealing with motion sickness is based on the use of desensitising
vestibular training, together with concomitant confidence-building counselling.
Persons who are suffering from severe incapacitating motion sickness are likely to
show some degree of anxiety or loss of confidence by the time they are referred for
a second opinion regarding their management and prognosis. This psychological
overlay seems inevitable, because these individuals are prone to develop a certain
degree of arousal in anticipation of the provocative motion stimuli that have previously led to motion sickness. In addition, professionals who experience motion
sickness feel that their careers are in jeopardy, and this adds to their anticipatory
anxiety; this feature is inevitably increased in those who are high achievers and will
be discussed later. This suggested that vestibular training alone would not be
enough; the arousal overlay would also require attention. As we shall see later,
success has been achieved in a high proportion of cases. Those who did recover
finished above the average, both during training and subsequently as aviators in
their operational squadrons.
Over the years my approach to overcoming the problems of motion sickness in
the Royal Air Force with the desensitisation training programme finally evolved
with the name of “Cognitive-Behavioural Desensitisation Training Programme”
and it will be discussed in some detail in Chap. 12; since then it has ben used
successfully with that problem, whatever the cause.
Current Version of RAF Desensitisation Programme: Since the time that I left
the Royal Air Force, fundamental changes have been made to my original programme. These changes provide an interesting insight into the key aspects of
handling motion sickness without resort to medication. For that reason this current
RAF desensitisation programme will be reviewed in some detail by way of
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contrasting it with the original version. I believe that this will give the reader a
better understanding of the various mechanisms involved, and ways of dealing with
this problem.
In January 1981, the RAF desensitisation training programme had been transferred from its original location at the (pre-flight) Initial Training School to the RAF
Institute of Aviation Medicine (IAM) at Farnborough. In 1985 Bagshaw and Stott
reported on changes that they had made during that time and I shall review that
description of their new version of the programme, and comment on their observations. Unfortunately, any changes that had been made between 1972, immediately after I left the RAF, and 1981 when the programme was in the hands of others
have not been documented, so they are not reflected in that review article published
by Bagshaw and Stott in 1985.
There have been no absolute pre-conditions for entry into the Bagshaw and
Stott’s version of the programme. Apparently they did, however, take advice from
the student’s flight training school concerning the trainee’s prospect of training
success once free from motion sickness. They also made an effort to exclude those
candidates who felt that they had made a mistake in choosing a career in flying.
Bagshaw and Stott stated that “some small degree of selection of subjects for the
course may take place before referral by the training units, but poor progress in
training is an almost inevitable accompaniment of continuing motion sickness and
due account is taken of this.” No exclusions whatsoever had been made in my
original desensitisation programme. This affects the comparative significance of the
ultimate results.
In the Bagshaw and Stott programme, subjects have undergone an initial
three-day assessment; this is another feature that had not been required in my
original programme. This assessment has included a detailed history of the individual’s pattern of motion sickness and an inquiry into “relevant psychological
factors.” Vestibular function tests have then been carried out to exclude the presence of any functional abnormality. This is an additional level of screening which
had not been present when the programme first started. The subject’s susceptibility
to motion sickness has then been evaluated by means of 3 provocative laboratory
stimuli; cross-coupled (Coriolis) stimulation involving active head movements in a
rotational environment, linear Gz oscillation (0.3 Hz, ±0.25 G) and angular
oscillation (0.02 Hz, ±150°/s), while carrying out a visual search task. An attempt
has been made to evaluate the subject’s rate of adaptation using a cross-coupled
(Coriolis) stimulus of gradual onset. That test was performed at the same time each
day, on three consecutive days, using identical stimulation. Apparently during the
three years prior to their report, no cases had been refused admission to the
desensitisation programme following initial assessment. This is perhaps not surprising since these flight trainees had already undergone a thorough medical
screening before being accepted for flight training. Indeed, this is the main reason
why I believed that this was not necessary when I first instituted my programme.
It is not clear from their report, however, whether or not any clients had been
rejected at some stage during that assessment.
11.1
RAF Desensitisation Programme
223
The types of stimuli used for ground-based desensitisation were the same as
those used for the evaluation of motion sickness susceptibility, whereas in my
original programme cross-coupled (Coriolis) stimulation alone was used. During
the three weeks of ground training, subjects had two sessions of training per day.
Up to one third of these might have been carried out on the vertical vibration
device, with an added visual task if the initial assessment had shown that a subject
was sensitive to linear Gz stimulation. In addition, subjects were given one session
per week of angular oscillation while performing a visual search task.
During cross-coupled stimulation, the subject was seated in an enclosed cab over
the axis of rotation and made active head movements in pitch and roll axes while
rotating in the yaw plane. The speed of rotation was increased in increments of
1-rpm while the subject made 5–20 sequences of head movements at each
step. A sequence of head movements entailed making 8 head movements at 3-s
intervals. The cab alternated every 5 s between light and dark. Every 30 s, after
each sequence of head movements, the subject reported his well-being rating
(WBR) on a scale of 1–6. Figure 2.1 meant “no symptoms” and the numbers
increased through malaise and increasing nausea, up to level 6, which would have
indicated emesis. The session ended when the subject reported a WBR of 4,
because the symptoms of motion sickness tended to escalate fairly rapidly beyond
that point. The stimulus dose for each session has been estimated by adding the
products of rotational speed (rpm) and the number of head movements at that speed.
The resulting numbers were plotted throughout the overall treatment as an indicator
of progress.
In this version of the RAF programme, cross-coupled stimulation was achieved
by the subject making active head movements in pitch and roll while rotating in
yaw. Previously, when desensitisation had been carried out using my chair, the
pitch and roll movements had been performed by the tilting of the subject’s chair,
providing whole body motion, and head movements had been achieved passively.
In addition, the subject now reported his well-being rating (WBR) on a scale of 1–6.
No such reports had been requested in the original RAF programme, I believed that
this type of reporting could have a negative effect on a subject’s confidence. I had
always ensured that the stimulus was carefully controlled so as to avoid excessive
motion responses, and made every effort to be positive and encouraging after a
desensitisation run. Therefore any questions relating to motion sickness had been
strictly avoided. In my original version of the programme confidence building
counselling had been an integral part of the technique; no mention of this is made in
the description of the present RAF programme.
Since the middle of 1981, subjects have also been exposed to linear Gz oscillation during the second week (or later) if they showed some increase in tolerance to
cross-coupled (Coriolis) stimulation. This has involved the use of a 2 m. stroke
vertical oscillating platform at 0.3 Hz (±0.25 Gz) and 0.4 Hz (±0.4 Gz) to provoke a motion response. The provocative stimulation has also been intensified by
giving the subject a visual search task to perform, without an external (Earth-fixed)
visual reference. The subject scanned a 2 12 matrix of numbers; the rows being
referenced by randomly ordered digits (1–12) and the columns by randomly ordered
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letters (A-L). On being given an alphanumeric coordinate, the subject was required
to respond with the appropriately referenced number, along the lines described in
the VVIT provocative test (Chap. 8). Two of these arrays were used, one above the
subject’s line of sight and the other on his or her knee. Since the subject was using
the arrays alternately this has promoted active head movements. Despite the prior
cross-coupled (Coriolis) exposure, Bagshaw and Stott had not observed any
increase in tolerance to the linear Gz stimulus above the baseline level established
during the initial assessment.
During one of the weekly sessions the subject was exposed to angular oscillatory
stimuli in yaw at 0.02 Hz (±150°/s). During this, the subject carried out the same
visual task described in the previous paragraph, but without head movements;
reading from a single array of numbers on the turntable. Preliminary observations
appeared to suggest that some increase in tolerance had been transferred from that
acquired on exposure to cross-coupled (Coriolis) stimulation. Progress during the
ground phase was considered satisfactory if subjects were able to make 20 head
movement sequences while rotating at 10 rpm, and could survive 20 min of 0.3 and
0.4 Hz Gz oscillation without developing more than mild symptoms of motion
sickness. Apparently the period of ground training had been extended on occasions
if these goals were not achieved, but no details have been provided in the review
article. The authors did state, however, that they considered the rate of progress and
degree of acquired tolerance during this phase of the treatment to be poor indicators
of a subject’s ultimate success in overcoming airsickness. This is an interesting
comment, because I have previously reported that the subject’s response during the
first week of training seemed to give a good indication of the ultimate outcome.
Bagshaw and Stott (1985) pointed out that all aspects of aircraft motion could
not be reproduced on the ground. For that reason, they considered that
ground-based desensitisation alone was not enough and should be regarded only as
an essential precursor to a period of graded remedial flying. This consisted of 10–
15 h flown in a jet fighter trainer with the Institute’s Medical Officer Pilot, who was
also a qualified flight instructor. An exception had been made in the case of flight
crews from maritime reconnaissance aircraft, which were given four more weeks of
ground-based desensitisation that contained additional sessions on the vertical
oscillator. This attitude constituted another fundamental difference from my original
cognitive-behavioural approach, in which success could be achieved by ground
training alone. Their remedial flight training programme consisted of a progressive
increase in motion stimulation from physiologically undemanding straight and level
flight to advanced acrobatic manoeuvres and high-speed, low-level navigation. The
syllabus was divided into initial and advanced phases, which were suited to the
needs of each subject.
The initial phase was similar for both pilots and navigators, but the advanced
phases differed in emphasis. Progress throughout depended entirely on the subject’s
rate of adaptation. There had been no pressure to achieve a particular objective
during each sortie. The initial phase usually lasted about five flight hours, during
which the subject often retained some sensitivity to provocative motion. However,
11.1
RAF Desensitisation Programme
225
once the subject could carry out a 60° angle of bank, level turns and circuit flying
with no motion sickness response, the advanced phase began.
During this phase of desensitisation, the subject learned to fly the aircraft to its
limits and, as Bagshaw and Stott pointed out, the subject’s confidence increased as
he or she began to regain the pleasure of flying. At the end of the advanced phase,
the subject carried out a navigation exercise during which the aircraft was landed at
the subject’s home airfield. Bagshaw and Stott considered that this provided the
final boost to the person’s attitude to rehabilitation since the subject was able to
restore self-esteem by showing off to his or her colleagues. They stressed that this
feature should not be underestimated. The advanced phase for navigators concentrated on low-level navigation and attack manoeuvres, ending with one-on-one air
combat.
During rehabilitation flying, subjects reported their WBR, just as they had done
during ground desensitisation training. Each sortie was given a “provocation
index,” on a scale of 1–6, based on the type of manoeuvre, ranging from straight
and level flight, with medium turns (rated 1), through an acrobatic sequence or
attack profile (rated 6). The subject’s “well-being rating” and the appropriate
“provocation index” were then plotted graphically to assess progress.
During the flying phase, it had been apparent that subjects varied in terms of
their pattern of progress. There was typically a gradual increase in tolerance as
motion provocation increased; however, on occasions it seemed to be more abrupt.
Apparently it had been rare for a clear indication of an adaptive response to be
absent during the flying phase. When the course of therapy had been completed,
subjects returned to flight training irrespective of the apparent outcome of treatment.
Even at that stage, Bagshaw and Stott considered that the prediction of a successful
outcome was not easy. These two flying phases, intrinsic to their desensitisation
training programme, have been added to what had been carried out in my original
method and were unique to Bagshaw and Stott’s version.
Bagshaw and Stott analysed the results of follow-up surveys for the periods
1974–1980 and 1981–1983. They classified the effects of their form of therapy
under five headings. The first two categories were related to those subjects whom
they considered to have been desensitised successfully and who have continued to
fly; subjects in category three were also considered to be successful since their
failure to complete flight training had been due to reasons other than motion
sickness. Category four subjects had suffered a recurrence of motion sickness.
However, they had completed flight training and their problem with motion sickness had been overcome by reassigning them to a different type of aircraft. Category
five subjects had failed to complete flight training on account of motion sickness.
They regarded subjects in the first three categories as therapeutic successes. On that
basis, the success rate for the period 1981–1983 had been 84%, compared with 70%
for the period 1973–1980.
Bagshaw and Stott particularly stressed that their approach to treating motion
sickness has been fundamentally physiological and that ground desensitisation was
designed to reproduce features of the neural mismatch that has been generated in
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the airborne environment. This represents the main shift of emphasis from the time
that I first described my original version of this technique.
In summary, the RAF desensitisation technique appeared to have changed some
time after 1972, when I left the Royal Air Force, from a cognitive-behavioural
training programme to what was now essentially a form of behavioural therapy with
little or no emphasis on cognitive counselling. In addition to the cross-coupled
stimulation used by myself, further training using linear Gz oscillation and angular
oscillation has been added and “the psychological aspects of treatment are not
strongly emphasised,” to quote Bagshaw and Stott. In addition, 10–15 h of high
performance, planned flying has been provided. In order to examine the implications of these changes in terms of the success and cost-effectiveness of the
programme, the new RAF programme and results will later be summarised and
compared with my original technique (Dobie 1974).
11.2
USAF Behavioural Airsickness Management (BAM)
Giles and Lochridge (1985) reported that the United States Air Force Behavioral
Airsickness Management (BAM) programme had been designed for student pilots
suffering from airsickness. It aimed to provide immediate treatment close to the
undergraduate pilot training site, and hopefully to return clients to flight training as
soon as possible. This programme included a combination of behavioural and
cognitive modification so as to reduce airsickness to such an extent that it did not
interfere with the student’s ability to fly the aircraft safely. Subjects were expected
to gain progressive relaxation skills so that they would be able to identify the
gradational onset of motion sickness, lower that threshold, and avoid associated
physiological distress by means of physiological relaxation and diaphragmatic
breathing. In addition, the researchers used cognitive restructuring techniques to
evaluate perceptual and problem-solving skills.
All potential candidates for the programme were first screened by a flight surgeon to exclude any underlying physical effects, or fear of flying, that might have
accounted for the subject’s airsickness. That interview also included a general
evaluation of the individual’s suitability for entry into the treatment programme. At
the time of the report, 37 student pilots, aged between 20–25 years, from the
subsonic (T-37 aircraft) phase of pilot training had undergone treatment in the
BAM programme; all had jet training experience of between 10 and 35 h.
Initially, the subjects’ history of motion sickness has been recorded in detail in
order to establish the individual pattern of recurrent airsickness. Subjects were then
given a standard progressive relaxation audiotape to use for practice at home. This
was followed by symptom management training, which consisted of incremental
exposure to increasingly severe provocative motion on a Bárány chair in order to
provide spatial disorientation and vestibular stimulation. During these training
sessions the students were encouraged to develop “self-initiated countermeasures”
to cope with the physiological responses caused by these provocative vestibular
11.2
USAF Behavioural Airsickness Management (BAM)
227
disturbances. A combination of diaphragmatic breathing and cue-evoked relaxation,
known as a “drop-off technique,” became the subject’s countermeasure for these
responses to the increasingly severe provocative motion. This rehabilitation training
programme took some 6–8 h of training on four or five successive days.
Giles and Lochridge reported that 37 students had been treated in the BAM
programme and 35 of these were then returned to their flight training programme.
Subsequently two of these had been eliminated by their operational units,
being diagnosed as having significant “fear of flying.” After one year, five of the
35 students continued undergoing flight training, an additional 12 were eliminated
from the programme because of shortcomings in their flying unrelated to airsickness, and 20 successfully completed their pilot training.
11.3
USAF Biofeedback Training
In 1979 Levy et al. (1981) designed the USAF School of Aerospace Medicine
Airsickness Treatment programme, based on physiological monitoring and
biofeedback relaxation. By mid-1980, 20 pilot trainees who had been disabled by
chronic severe airsickness entered and completed this programme. The managers of
the programme stressed that those prospective candidates for the programme must
be selected very carefully in order to ensure that they were highly motivated. In
addition, they have been given a thorough medical screening to rule out the presence of any other conditions that would have called for medical disqualification.
This procedure is in contrast to the eligibility for entry into my original
cognitive-behavioural anti-motion sickness training programme, which did not
include any of these special constraints.
The premise underlying the USAF programme has been that the motion sickness
response was mediated through the autonomic nervous system and by learning to
control this autonomic activity, that response could be stopped. The candidates
were trained to use various relaxation techniques and desensitised in a rotating/
tilting chair, which provided passive provocative Coriolis stimulation. In the
treatment plan, the patients have never been stimulated to the point of frank
vomiting, although apparently this had happened on five occasions. Both the patient
and the flight surgeon psychiatric investigators constantly monitored the patient’s
psychological responses to provocative motion. The patients learned to control and
abort this (autonomic) motion sickness response to cross-coupled (Coriolis) stimulation through exercising autonomic control. You will have noticed that they have
used the word “patient” and “treatment” which reflects a difference in our attitudes
to this problem. After completing the programme, every effort was made to return
the candidate to flying within 3 days, since the investigators believed that further
delays could have an adverse effect on the outcome. The candidate was then given
5 trial flights involving increasing stressful content before undergoing the sixth
check flight. If this flight has been deemed to be satisfactory, the candidate was then
returned to flight status.
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Levy et al. reported that following their treatment, one of the 20 patients was
permanently grounded for medical reasons entirely unrelated to motion sickness;
two were dropped from flight training because of continuing motion sickness; one
had withdrawn from radio operator flight duties due to persistent motion sickness;
and 16 returned to full flight status (a success rate of 84%). Levy et al. pointed out
that, prior to the use of biofeedback, the USAF School of Aerospace Medicine
airsickness treatment programme had “a return-to-duty rate of only 45–50%.”
These results have been based on a select population, however, and there was no
information on the long-term outcome.
After Levy left the group, Jones et al. (1985) followed up the progress of the
USAF School of Aerospace Medicine biofeedback-moderated behavioural treatment programme, which Levy et al. (1981) had reported some four years earlier. In
particular they stated that, to their knowledge, this programme represented the first
time that relaxation techniques had been taught “in a dynamic and challenging
environment,” as distinct from the low-stimulus situation more typical of clinical
biofeedback training. In their opinion, biofeedback training might help those suffering from motion sickness in at least two ways, by checking involuntary autonomic responses to provocative motion and by reducing associated anxiety. Since
the original report, the programme had continued to accept only candidates who
were considered to be well motivated. Each subject has been trained in a number of
relaxation techniques and has learned the basics of deep muscle relaxation using an
abbreviated version of Jacobsonian contraction and slow relaxation (Jacobson
1938). In addition, they were taught the fundamentals of diaphragmatic breathing
and relaxing mental imagery.
The biofeedback instrumentation recorded skin temperature on the surface of the
distal fleshy aspect of the middle finger of the left hand, the skin conductance level
and skin conductance response at the same distal locations on the second and fourth
fingers, and electromyographic data from the standard forehead placement over the
frontalis muscle. These physiological recordings were made while the subject has
been exposed to incremental increases in cross-coupled (Coriolis) vestibular stimulation in a rotating/tilting chair. Each subject was given approximately 20 sessions
of Coriolis stimulation. Each session lasted some 30–45 min. and took place twice
per day, in the morning and afternoon, during two workweeks. When a subject has
shown signs of habituation to a particular level of provocative stimulation, the rate
of rotation was increased and/or the provocative motion challenges took place
closer together. The aim of the programme was not merely to increase a subject’s
tolerance to cross-coupled (Coriolis) stimulation; rather it has been for the person to
suppress nausea as quickly as possible by thinking about something else. Subjects
who described particular dislikes, such as the smell of fuel, were instructed to use
mental imagery to visualise these products while practicing their relaxation techniques, which made use of the principles of Wolpe’s systematic desensitisation
(1973). Jones and Hartman (1984) stressed that relaxation was essential to the
success of biofeedback therapy. They made the point that the patients could continue to practice these techniques at home, and those who did so were likely to be
more successful than the others.
11.3
USAF Biofeedback Training
229
Following their course of treatment, five reorientation flights as a supernumerary
crewmember were programmed for each flight trainee. The concept underlying this
phase of the programme has been to exclude the subject from any responsibility in
flight and thereby allow him or her to practice relaxation techniques in the air. This
is a somewhat different protocol to that described by Levy et al. (1981). The first
flights were, however, carefully controlled along the lines suggested by myself in
1974, in order to avoid undue motion stress, on the immediate return to flying, after
spending a long period on the ground.
Jones et al. (1984) reported on the results of this USAF biofeedback programme
for the period from August 1979 through June 1984. During that time, 63 fliers had
been evaluated to assess their suitability for treatment. Of these, 53 underwent
treatment during the period August 1979 to June 1982. Each subject was followed
for two years after the completion of treatment. Success has been defined as
returning to and maintaining satisfactory operational flight status. They reported
that of these 53 fliers, a total of 42 (79%) met this criterion; a further three (6%)
were considered to be partially successful, and eight (15%) have subsequently been
grounded due to recurrent airsickness. Of those who had been regarded as partial
successes, recurring airsickness had caused two to be reassigned to transport aircraft
and the third had eliminated himself from flying after a year, because of airsickness
during low-level sorties. It should be pointed out, however, that these results have
been achieved in a highly selected population, since 8 of those referred did not pass
the acceptance screening. You will also have noticed that these subjects had always
been referred to as patients; that was never done with subjects in our programme
because, as I have already said, that might tend to remind them of an illness and that
was something that we always avoided. This matter will be addressed again later
when discussing the results of my original cognitive-behavioural training programme for RAF flight trainees.
A year later, Aitken and Benson (1984) reported on the use of relaxation/
desensitisation therapy, which they described as revised systematic desensitisation,
for treating anxiety in 47 navy flight trainees; 46 of whom were male and 1 female.
The reasons for referring these students to the Psychiatry and Neurology Service at
the Naval Aerospace Medical Institute at Pensacola ranged from a diagnosis of
“excessive anxiety” to that of “airsickness resulting from anxiety.” The candidates
in the programme attended a series of 3–6 one-hour sessions of relaxation/
desensitisation therapy, with at least one day between each appointment to allow
time to practice the techniques learned during the previous session. This form of
therapy has used a behavioural approach, and included relaxation exercises and
in-depth mental imagery.
A follow-up evaluation after six months found that 79% of the subjects had
successfully completed their flight training. Aitken and Benson also pointed out that
within that overall group, 13 of the 14 subjects who entered the programme,
following a thorough psychiatric screening, had successfully completed flight
training (93%), compared with only 24 of the 33 subjects (73%) who did not have
such pre-screening.
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Benson and Aitken (1985) later reported a three-year follow-up study of 34 out
of a total of 37 patients who had been treated for flight anxiety by means of
behavioural relaxation/desensitisation therapy. They found that 26 of these subjects
(77%) were still flying actively. Benson and Aitken then discussed the differences
between the successes and failures, as well as the long-term value of this type of
treatment. In their initial follow-up, they noted significant differences on Minnesota
Multiphase Personality Inventory (MMPI) scale elevations and the patients’ major
presenting symptoms. They reported a significant relationship between specific
MMPI profiles, namely, the validity scale “frequency” F (a tendency to exaggerate
complaints) and the following clinical scales, Hs (hypochondriasis), Hy (hysteria),
Pa (paranoia), Pt (psychasthenia), and Sc (schizophrenia), and a failure to treat
flight anxiety successfully. These profiles were considered to denote as much
tension during treatment as had existed in flight (Spielberger 1996). Benson and
Aitken have, therefore concluded that the patients most likely to benefit from this
form of therapy were those who have exhibited normal MMPI profiles, and whose
major presenting problem was their airsickness.
Li et al. (1991) also reported on a study in which they used biofeedback and
imagery exercises to treat anxiety in 26 male student pilots, aged 20–22 years. The
clients have been divided into experimental and control groups. The experimental
group was given 16 thirty-minute sessions of biofeedback and imagery training,
using an audiotape, after successive training flights. The imagery training was
related to the events of the flight. On non-flying days, the subjects underwent
auto-relaxation exercises. The control group carried on with their normal flight
training programme, without any additional procedures. Li et al. reported that the
exercise group performed much better than control in both flying and visual search,
and none had been grounded due to recurring anxiety. On that basis they concluded
that this technique had been a useful and practical method of managing student
pilots who exhibited signs of anxiety.
11.4
Canadian Forces Airsickness Rehabilitation
Programme
The Canadian Forces (CF) rehabilitation programme began in 1981 with the
installation of ground-based desensitisation equipment. Banks et al. (1992) reported
that it contained elements common to both the RAF and USAF programmes, both
of which have just been described.
The then current CF policy stated that if a pilot trainee had experienced airsickness that led to vomiting despite the use of a mixture of Phenergan® (25 mg)
and ephedrine (30 mg), administered 60–90 min before flight, or if vomiting
occurred during flights subsequent to the maximum permissible three dual-only
flights on medication, the trainee was grounded and given rehabilitation training.
The programme first consisted of identifying candidates who were suitable for
treatment, rehabilitation, and post-treatment follow-up, either by self-referral or on
11.4
Canadian Forces Airsickness Rehabilitation Programme
231
the recommendation of flight-line instructors. Non-pilot flight crewmembers were
also eligible for the programme. When potential candidates were being considered
for treatment special attention has been paid to personality factors, stress evaluation
and the individual’s motivation to fly. Those subjects who were selected for
rehabilitation have undergone a three-phase training programme that consisted of
biofeedback relaxation therapy in phase 1, followed by ground-based desensitisation (phase 2), and, finally, in-flight desensitisation (phase 3). This pattern of
training showed the combination of the USAF and current RAF techniques.
Subsequently, the success of the programme has been evaluated by means of an
informal periodic follow-up.
In the first phase, subjects were taught deep muscle relaxation using the methods
described by Jones et al. (1985). They were given a biofeedback device and
instructional tape and taught how to use them. After two days of relaxation training,
the subjects proceeded to the second phase of training. They also continued
relaxation therapy throughout the next two phases of the programme.
During phase two, subjects underwent ground-based desensitisation, which
consisted of cross-coupled (Coriolis) stimulation by making active sequential
fore-and-aft and lateral head tilts while seated on a rotating platform. The subject
was monitored by means of electrodermal activity measurements in order to assess
his or her ability to cope with provocative stimulation. This was achieved by measuring galvanic skin resistance, recorded by finger sensors, and relayed to an external
control panel to give the therapist an indication of the subject’s state of tension or
relaxation. The programme began at a rotational speed of 6 rpm and subjects
repeated the sequence of head movements 10 times at a rate of one every 4–6 s.
When completed, the subject positioned his or her head normally and provided a
magnitude estimate of motion sickness symptomatology on a rating scale of 1–10.
This conflicts with my philosophy, since it appears to reinforce failure rather
than encourage a feeling of achievement. This rating is that which had previously
been employed by Jones et al., where “1” has represented a symptom-free condition, “10” recorded frank vomiting, and intermediate scores indicated the subject’s
estimate of the degree of motion-induced discomfort. If the subject’s assessment of
his symptoms provided a rating of less than 5 or 6 (sweating, mild disorientation,
stomach awareness), the rate of rotation has been increased by 2 rpm and the
exposure was repeated.
The therapist monitored the subject continuously and compared his or her
magnitude estimates of symptoms with the galvanic resistance indicators of
apparent relaxation or tension. According to these findings, the therapist coached
the subject on relaxation and ended the session when he or she could not keep the
symptom rating below 6 or 7. Therapeutic sessions were given twice daily, seven
days a week, until a rotational speed of 20 rpm had been reached. At that stage the
subject wore flight gear during the desensitisation sessions and various random
changes have been introduced in terms of environmental factors and manipulation
of the provocative stimulation. That procedure was also adopted in my original
programme. Banks et al. stated that these variations to the basic programme have all
been aimed at emphasising “mastery of the environment.”
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After completing ground-based desensitisation, subjects underwent the final
phase of therapy, which normally consisted of 6 desensitisation flights in a
Canadaire CT-114 Tutor basic jet trainer. The student flew the aircraft within the
limits of his or her capability and was supervised by a qualified pilot who could also
act as a rehabilitation therapist. During the first flight, manoeuvres were avoided to
control provocative stimulation to ensure completion of the sortie without motion
sickness. During the rest of the flights, the subject was exposed to incremental
increases in provocative stimulation, tailored to his progress. Should the pilot
supervisor consider that it had been necessary on any particular sortie, however,
supportive therapy that emphasized relaxation was also included.
Banks et al. reported an overall success rate of 77.3% for their airsickness
rehabilitation programme and concluded that a programme of desensitisation for
student aviators suffering from severe airsickness was a valid and practical clinical
tool. These particular results will be reviewed later, with those from other motion
sickness programmes that have been or are being used in other military settings.
11.5
US Navy Motion Sickness Prevention Programme
Based on Transfer of Adaptation
Graybiel and Knepton (1978b) reported on a programme in which they sought to
prevent airsickness during aerial manoeuvres by transferring protective adaptation
to provocative motion that had been obtained in a laboratory setting by carrying out
head movements during rotation in a slow rotation room (SRR). In a previous
experiment, Graybiel and Knepton (1972) had already demonstrated evidence of
subjects acquiring direction-specific adaptation following active head movements in
a slow rotation room. This adaptation effect decayed spontaneously after a few
hours to reveal a non-directional-specific adaptation that lasted some days. In
another study Graybiel and Knepton (1978a) reported that, in some subjects,
bi-directional over adaptation has also been shown to occur following head
movements to the left or to the right during unidirectional rotation in a slow rotation
room.
In this latest programme under review, 10 aviators had been referred to the Naval
Aerospace Medical Research Laboratory as possible candidates for protective
adaptation to cross-coupled angular accelerations in a slow rotation room, following
grounding due to nausea and vomiting. However, only 8 of the 10 subjects were
available to undertake this training; one was dropped from the programme on
psychiatric grounds and the other had decided that he could no longer tolerate
motion sickness. The plan of the programme was as follows:
(a) initial interview:
(b) review of personal health and flight documents;
(c) assessment tests of motion sickness susceptibility in SRR;
11.5
US Navy Motion Sickness Prevention Programme Based on Transfer …
233
(d) provisional adaptation schedule in SRR, with or without anti-motion sickness
medication.
(e) assessment of transfer of adaptation from practiced (counterclockwise) to
unpracticed (clockwise) rotation in SRR,
(f) assessment of protection against provocative motion in actual flight,
(g) follow-up history.
The main consideration for using anti-motion sickness medication during
adaptation training has apparently been based on a subject’s marked susceptibility
to motion sickness in the SRR and the efficacy of a combination of the drugs
promethazine and ephedrine at fixed doses of 25 mg each in those subjects. Of the
8 subjects who were admitted to the programme 6 were given that drug combination during adaptation training. Of those 6 candidates, 4 had returned to flying
and 2 had not. Of those 2 who did not receive drugs, one was grounded and the
other returned to flight status. On this subject of using anti-motion medications
during adaptation training, the researchers felt that this was an important decision
that had not been given enough attention at the time. My personal feeling is that it is
better to reduce the severity of the training stimulus, so as to avoid the need for
drugs, but this is an issue that requires further study.
Graybiel and Knepton reported that 5 of the 8 subjects (62.5%) who had
undergone adaptation training regained their flight status, based upon follow-up
reports after periods of time ranging from 10–27 months. These results have been
included in Table 11.1 later in this chapter (USN 75–78). Unfortunately, it has not
been possible to make a direct comparison of these results with others shown in the
table because we do not know what kind of aircraft these 5 individuals had been
flying when the follow up reports were received; nor can we identify the various
durations of follow-up for each of the 5 individuals.
11.6
US Navy Self-paced Airsickness Desensitisation
(Spad)
The US Navy has used a self-paced airsickness desensitisation programme (SPAD)
to try to recover those students who have experienced recurrent problems with
airsickness. It has been recommended that a minimum of four episodes of airsickness in student naval aviators/student naval flight officers and designated
aircrew have occurred prior to initial evaluation in order to allow time for natural
adaptation. Those personnel who have not tolerated the aircraft motion have then
been referred to the local flight surgeon. The initial evaluation has been planned to
investigate possible medical causes for airsickness. If referral to a specialist was not
indicated, the flight surgeon could then diagnose airsickness due to mal-adaptation.
If there have been no contraindications, 4 dual flights with an instructor should then
have been authorised with the addition of suitable medication. This should consist
of an oral combination of promethazine HCl (25 mg) and ephedrine (25 mg) taken
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60–90 min prior to flight. The student and the flight instructor should both be
briefed on the possible side effects of these medications. If airsickness has continued while on medication or recurred after the trial of medication has been
completed, the flight surgeon should then have referred the individual for self-paced
desensitisation therapy (SPAD).
In this programme, students were instructed in techniques of biofeedback. They
were then given 10 one-hour sessions over the course of a week. Along with
relaxation techniques they learned to control their heart rate, skin temperature, and
skin conductance. Students were then exposed twice daily to complex angular and
linear acceleration stimuli generated by active head movements performed while
rotating on a chair. The rotating chair was equipped with remote-controlled electronic circuitry that allowed the student to select the rate of rotation (rpm) at which
to make a series of head movements. Since the magnitude of the accelerative
stimulus from each head movement was proportional to the rpm of the chair, the
student was allowed to select the rate that was best suited to his or her adaptive
progress to this form of motion stress.
The students were scheduled for a 1-hour training session on the chair both in
the morning and afternoon, with a 3 h break in between. Each session consisted of
six 10 min sequences consisting of 5 min of head movements at a selected rpm,
followed by 5 min of rest during which the head has been kept immobile while the
chair rotated at the same rpm. Before and after each head movement sequence,
the client was asked to rate his or her motion sickness symptoms on a scale of
0–4 where: 0—no symptoms, 1—“uneasiness”, fatigue, headache, 2—stomach
awareness, mild nausea, hot, sweating, 3—increased nausea, increased salivation,
belching, 4—vomiting.
The student was required to closely monitor the symptoms of motion sickness to
prevent vomiting. If the student perceived that vomiting was imminent, the
immediate action has been to stop making head movements and keep the head held
steady against the headrest. After completing a sequence of head movements and its
associated rest period, the student might then either adjust the velocity to a desired
rpm by increasing the chair velocity by 2 rpm, stay at the same rpm, or decrease the
chair velocity by any multiple of 2 rpm. If the student had not been able to complete
all the head movements associated with a given sequence, he or she should have
kept the head still until the end of the entire sequence. For the next sequence, the
chair velocity should have been decreased by 4 rpm below the speed at which head
movements had been stopped.
At the beginning of the desensitisation programme, students were required to
begin each testing session at a relatively low rpm. On following days, they were
allowed to start each training session at a velocity not to exceed the maximum
velocity reached on the previous morning session, less 2 rpm in the chair.
The objective of this programme has been for the students to closely monitor
their motion sickness symptoms at all times and to gradually build up their tolerance to provocative motion through repeated exposure to gradually increasing
levels of stimulation on either the rotating/tilting chair or in the optyokinetic drum
(see Chap. 13). The rate of progress was solely up to the student, although most
11.6
US Navy Self-paced Airsickness Desensitisation (Spad)
235
students took some 6–8 weeks, 40–60 sessions, to complete the programme.
Successful completion of the programme was achieved when the student could
tolerate 20 rpm for 1 h without symptoms. Students were not to experience vomiting; since that indicated a failure to monitor their symptoms adequately.
After completing desensitisation therapy, the subject was returned to flight duty.
Several non-graded familiarization flights were undertaken within seven days of
returning to duty to allow the individual to re-establish familiarity with the aircraft
as well as incorporating learned coping skills into flight training. If subsequent
airsickness occurred, and affected flight performance, the student or aircrew
member was then removed from flight status.
As far as results are concerned, there is no current information available.
However, Bower et al. (1975) did submit an abstract on this subject to the 64th.
Annual Scientific Meeting of the Aerospace Medical Association that provided
some incomplete results for the programme during the period 1 January 1990–1
July 1992. They reported that 65 individuals had successfully completed the programme out of the 71 who had been enrolled; however, they had only been able to
contact 51 of those individuals for the purposes of this follow-up. No information
was given for the cause of failure of the 6 (8.5%) who were unsuccessful. Fourteen
of those who had graduated from the programme were still in training at the time of
reporting. They further recorded that of the 16 designated aviators they had contacted, 2 were piloting tactical jets, 3 multiengine transports and the remaining
11 were piloting helicopters. Of those who had been returned to their squadrons,
3 were disqualified from flight status for reasons other than airsickness and a further
11 (16.9%) disqualified due to continued airsickness. However, it is not absolutely
clear if that accounted for all those who were returned to their squadrons. In the
abstract they only reported on 44 out of the 51 individuals they had contacted, so
we do not know what happened to the missing 7 individuals. Since these results are
incomplete and I have been unable to obtain any results since then, the SPAD
programme is, regrettably, not included in Table 11.1, later in this chapter, in which
the results of various other military programmes are reviewed.
11.7
Autogenic-Feedback Training
NASA has used autogenic-feedback training (AFT) to treat motion and space
motion sickness. Using operant conditioning to train subjects to control their
autonomic responses is commonly called biofeedback; autogenic therapy uses
cognitive imagery to control responses that usually are involuntary. AFT is a
combination of both biofeedback and autogenic therapy, and is thought to be
considerably more effective than either of these two techniques alone.
Cowings (1990) pointed out that the rationale for using AFT to treat motion
sickness was based on the presence of significant changes in the autonomic nervous
system that were involved with this malady. The autogenic exercises were intended
to give the subject both instructions and a means of mental concentration likely to
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produce the optimal corrective response more quickly than trial and error.
The biofeedback component of the technique was intended to augment these
autogenic exercises by giving the subject immediate sensory information about the
magnitude and direction of that response, so as to increase the likelihood of making
the correct response. Both visual and verbal feedback were presented to the subject
for each of the autonomic variables (heart rate, respiration rate, plethysmography of
the finger and of the skin adjacent to the mouth, skin conductance of the fingers,
and electromyographic activity in the intercostal muscles). During a training session, the subject practiced controlling these physiological responses from the different feedback display presentations, while being exposed to provocative motion
by means of cross-coupled (Coriolis) stimulation.
In their preliminary study, Cowings et al. (1988) evaluated autogenic feedback
training (AFT) for the treatment of the Space Adaptation Syndrome on Space-Lab
3. Four astronauts had taken part in that trial. The treatment subjects, crewmen
A and B, were given pre-flight training in the control of heart rate, respiratory rate,
peripheral blood volume, and skin conductance. The other two subjects, C and D
served as controls and as such received no AFT training. The researchers reported
that crewman A had shown that he was able to control his own physiological
responses reliably and that, following AFT training, he showed a significant
increase in his tolerance to motion sickness. On the other hand, crewman B, who
had been less able to control his responses, showed only a moderate increase in his
tolerance to motion sickness after similar training. The reports of their symptoms
during flight in space, together with the recordings of their physiological responses,
demonstrated that Crewman A had not experienced severe motion sickness,
whereas Crewman B had reported one severe bout of motion sickness. Both subjects in the control group, who were given anti-motion sickness medication,
reported that they had experienced numerous episodes of motion sickness on the
first day of the mission. Based on both the in-flight physiological data and the
subjective reports from the astronauts, Cowings et al. concluded that autogenic
feedback training might be an effective means of preventing the effects of space
motion sickness. However, further data must be obtained in-flight before a final
decision on the effectiveness of this form of therapy could be made.
Cowings et al. (1990) continued their efforts to develop a method for treating
motion sickness based on a subject’s ability to regulate the activity of heir autonomic nervous system. In this study they examined the reproducibility of the
patterns of the autonomic responses of various subjects exposed to provocative
motion. They induced motion sickness in 58 healthy subjects (47 males and
11 females) by means of standardized active head movements while the subjects
rotated in a Stille Werner rotating chair. The Coriolis Sickness Susceptibility Scale
(CSSI) developed by Graybiel et al. (1969) was administered to the subject every
5 min in order to standardise the level of malaise throughout the trials. A simple
global diagnostic score could then be derived from the CSSI self-report information
and experimenter data.
In addition, they measured the following physiological responses: heart rate,
finger pulse volume, respiration rate, and skin conductance. In order to compare the
11.7
Autogenic-Feedback Training
237
responses across different autonomic system variables, they used standard scores to
examine the stability of the autonomic responses of specific magnitudes across both
of the provocative tests, as follows: difference scores were calculated by subtracting
the pre-test means from the means for each of the four test periods. Since the length
of exposure for each provocative motion test has varied, only selected periods
common to all subjects were used. A positive sign has indicated increased sympathetic activity.
Comprehensive statistical analyses showed marked, stable, individual differences in the autonomic nervous system responses to both mild and severe motion
sickness. Cowings et al. postulated that their findings have confirmed their prior
observation that different people have their own unique autonomic nervous system
responses to motion sickness. For that reason they believed that it was necessary to
provide each individual with his or her own personal, self-regulation training
programme.
In a series of laboratory experiments Cowings et al. (1988) showed that subjects
given AFT withstand provocative motion in the form of cross-coupled (Coriolis)
stimulation, longer and at higher rotational values than the control subjects who had
not been treated. These subjects had been trained to control numerous autonomic
responses under both resting and provocative motion conditions. In addition,
Cowings et al. reported that the protective effect has transferred successfully to
other forms of nauseogenic motion, both real and illusory.
11.8
Evaluation of Autogenic Training and Biofeedback
Jozsvai and Pigeau (1996) investigated the effect of autogenic training and
biofeedback on a person’s tolerance to motion sickness. Following their review of
that literature they made a number of observations. First, if biofeedback has helped
a person to regulate his or her autonomic nervous system, that learning should be
improved if the autogenic training has been supported with true feedback rather
than false feedback. Second, if autogenic feedback training has been effective in
dealing with motion stress, the addition of true feedback should have improved a
person’s tolerance to provocative motion, and have reduced symptoms of motion
sickness, than would have been the case with either false feedback or no training
whatever. Finally, they postulated that if a relationship has existed between
self-control of the autonomic nervous system and the ability to cope with motion
stress, there should have been a significant correlation between the degree of control
over the autonomic nervous system responses and the amount of provocative
motion that could be tolerated, and the severity of an individual’s symptoms of
motion sickness.
Their study included 18 students, aged 18–45 years, who were prone to motion
sickness. Provocative motion was induced by means of Coriolis stimulation using a
rotating chair with a headrest that has passively moved the subject’s head forward
and backwards over a period of 4 s. The visual stimulation provided for the
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feedback part of the experiment came from a television monitor attached to the
chair. Regarding autonomic nervous system responses, skin temperature was
measured on the index finger and heart rate from an electrode placed to the left of
the sternum at the level of the first rib. These physiological responses were fed back
to the subject both as auditory and digital signals. When the subject’s mean skin
temperature had decreased or increased by half a standard deviation from the
average at rest, a 2 s auditory signal has been triggered. At the same time, the visual
display has indicated either “attention, cooling” or “good, warming”, as appropriate. Heart rate responses were fed back to the subjects in similar fashion. In terms of
false feedback, this information has come from a videotape source.
The subjects have been divided into three groups, with six subjects in each
group, and they were given weekly exposures to cross-coupled provocative stimulation over a period of six weeks. After the first session, the subjects were
randomly assigned to one of three groups, which consisted of either true or false
feedback autogenic training, or served as control. Between the first and second
provocative stimulation sessions, the two autogenic training groups received four
consecutive daily sessions of autogenic feedback each lasting some 36 min. The
control group was exposed to the same experimental conditions, without being
required to perform any particular exercises, nor were they provided with any
feedback on their physiological responses.
The results of this study have shown that the subjects in both the true and false
autogenic-feedback training groups were able to increase their skin temperature and
heart rates, unlike the control groups, which have shown no such significant
changes. The learned control of skin temperature and heart rate in the two training
groups, however, did not show any relationship to their severity of motion sickness
nor their ability to withstand cross-coupled (Coriolis) provocative stimulation following their treatment.
Jozsvai and Pigeau reported that, although able to control autonomic nervous
system responses, the subjects were not able to do so in the provocative motion
environment, or if they have been able to do so, this control has had little effect in
protecting them from motion sickness or their ability to withstand the effect of these
cross-coupled stimuli. This has led to their conclusion that these findings did not
support the claim made by Cowings that the ability to regulate one’s autonomic
nervous system responses provided an effective means of being able to cope with
motion sickness. These observations are similar to the results that my colleagues
and I had obtained when evaluating the effectiveness of a clinical biofeedback
technique to manage motion sickness (Dobie et al. 1987). In that experiment, the
subjects in the biofeedback group were able to control EMG activity through
biofeedback, but apparently that provided little protection against the effects of
illusory motion. This will be discussed later in Chap. 13 when we evaluate
cognitive-behavioural training.
11.9
11.9
Review of Military Desensitisation Programmes
239
Review of Military Desensitisation Programmes
Unfortunately it is very difficult, if not impossible, to compare the results of the
different military desensitisation programmes because, as previously reported,
unlike my original programme all of these others have included some form of
pre-selection. This means that many of the subjects who have been listed as failures
in my programme might well have been precluded from entering my programme at
all, if the same pre-selection rules, as in these other programmes, had been applied.
Unfortunately, the number of potential candidates who had been excluded from the
other programmes was not made clear, however, because no specific figures had
been given. So we were unable to predict the success rate that would have been
achieved by these programmes if, in fact, there had been no form of pre-selection.
In addition, other desensitisation programmes are more complex than my
cognitive-behavioural programme. For example, the USAF biofeedback programme and the Canadian Forces (CF) airsickness rehabilitation programme require
additional instrumentation to record electromyographic data for biofeedback
training. In addition, I hold the firm conviction that the use of recording instrumentation can have a detrimental effect on a subject’s attitude of mind. It seems to
conflict with the emphasis being placed on the normality of the motion sickness
response. Professionals, especially, who have a motion sickness problem can be
suspicious of these physiological measures in terms of how the results will be used.
For the same reason, I prefer that counsellors are not associated with the practice of
psychiatry, because this again conflicts with the concept of routine training to
overcome a normal protective response; on the contrary, it hints of some neurotic
element.
The current RAF programme has been considerably modified since it was first
conceived by me. It now includes linear Gz oscillation and angular oscillation in
addition to the cross-coupled (Coriolis) stimulation used in the original
cognitive-behavioural training programme. Perhaps this reflects the virtual elimination of the cognitive component in the current RAF programme and the impact
that has on stimulus generalisation. The other military programmes use a form of
questionnaire to assess motion sickness symptomatology after provocative motion
exposures. During desensitisation training in my cognitive-behavioural programme,
this is specifically avoided, as already stressed. I believe that this has an adverse
effect on the subject’s confidence since it tends to reinforce failure. In terms of
rehabilitation flight time, the Canadian Forces programme normally consists of six
flights in a basic jet training aircraft, which is similar to my early RAF proposals
when I was thinking about a few uncomplicated fights for adaptation, due to the
layoff from flying. In the current RAF programme, however, this has been increased
to include special rehabilitation flying in a designated high performance aircraft.
The published results obtained during the three phases of the RAF programme
(my original pre-1974 programme), the interim years 1974–1980, and Bagshaw and
Stott’s 1981–1983 programme are shown in Table 11.1, along with those from the
USAF (Giles and Lochridge 1985), CF (Banks et al. 1992) and the US Navy motion
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sickness prevention programme based on transfer of adaptation (Graybiel and
Knepton 1978b). As stated earlier in the chapter when discussing the US
Navy SPAD programme, it has been omitted from this table because there are
insufficient data to permit the calculation of successes and failures. Unfortunately,
there is also little information on the long-term follow-up in a number of these
programmes.
It is evident that all of these military programmes are effective. However,
apparently none of these newer programmes have improved upon the success rate
of my original programme, despite the additional efforts and extra costs involved.
This calls into question the value of complicating the relative simplicity of the
original cognitive-behavioural approach, quite apart from the significant cost
increases that are involved in so doing.
11.10
Independent Comment on Desensitisation
Programmes
Jackson (1994) has pointed out that these various desensitisation programmes give
independent support to managing student pilots who have been suffering from
airsickness, by means of psychologically based techniques. Although this is
important, Jackson stressed that most of these approaches concentrated on
managing the problem and made little or no impact on better understanding the
cause of airsickness. In Jackson’s opinion, I had been the only one to offer a method
of treatment that was based on an implicit theory. For that reason, he suggested that,
in these other programmes, “any gains in airsickness management must be
implemented in a reactive rather than a preventive fashion” and did not allow
reasonable testing of the aetiology of motion sickness because they failed to propose an underlying theory.
Jackson has opined, however, that it was perhaps too critical to state that these
other clinical programmes provided little understanding of the causes of airsickness;
it was possible to make reasonable deductions about the various factors that contributed to this syndrome. Biofeedback, relaxation, and cognitive training improved
the symptoms of airsickness, so Jackson postulated “certain sensations, tension
behaviours, and disturbing thoughts are related to the rise of this condition.” He also
added that, since exposure to provocative motion stimuli caused improvement, this
suggested that “there is either some physical tolerance or, as Dobie et al. (1989)
speculated, that the motion environment provides an opportunity to practice and test
recently learned psychological strategies.” Jackson has suggested at least four
variables that appeared to be related to the onset and reduction in the severity of
motion sickness, namely, “sensation, behaviour, cognition, and physical factors.”
Jackson has then offered two general approaches to the management of motion
sickness. The first is to reduce as far as possible the effects of vestibular hypersensitivity by means of flying practice together with the use of anti-motion sickness
drugs (Wovters et al. 1983). The second is to employ a form of motion
11.10
Independent Comment on Desensitisation Programmes
241
desensitisation in combination with counselling, such as that which is proposed in
my cognitive-behavioural anti-motion sickness training programme (Dobie 1974).
Jackson concluded that since the symptoms of airsickness are best managed without
the unwanted primary and side effects of medications, “the behaviourally based,
biologically affected strategies should take precedence.” That was a very interesting
evaluation of the various forms of the management of motion sickness given by
Jackson.
11.11
Other Methods Used to Treat Motion Sickness
Slow Deep Breathing: Jokerst et al. (1999) carried out a study to investigate the
hypothesis that slow deep breathing, at approximately 8 breaths per minute, would
prevent gastric dysrhymias and symptoms of motion sickness during exposure to
illusory motion in an optokinetic drum. Respiration was monitored by mercury
strain gauge to confirm breathing frequency in the experimental condition. Motion
sickness symptomatology was obtained prior to and during drum rotation using a
questionnaire based on that developed by Graybiel et al. (1968). They found that
slow deep breathing had decreased the symptoms of motion sickness.
Acupuncture: Hu et al. (1992) have reported that acupuncture has been used in
China for many years to treat gastrointestinal symptoms. Apparently nausea and
vomiting are commonly treated using the acupuncture point P6, which is the Nei
Kuan point. This lies 2 Chinese inches proximal to the crease on the wrist between
the tendons of palmaris longus and flexor carpi radialis. A Chinese inch is apparently the length between the creases over the proximal and distal interphalangeal
joints of the middle finger in flexion. Hu et al. notes that Dundee et al. (1986) have
reported that the use of acupuncture at the P6 point for a period of 5 min immediately following premedication with opioids reduced postoperative nausea and
vomiting in patients undergoing minor gynecological surgery. Dundee et al. (1989,
1987) have later employed electro-acupuncture at the same P6 point and found that
it reduced nausea and vomiting in cancer patients undergoing cisplatin therapy.
Acupressure: As distinct from acupuncture, acupressure has been used later in two
studies (Warwick-Evans et al. 1991; Bruce et al. 1990), but failed to ameliorate
motion sickness. Acupressure has the advantage of being noninvasive and could
therefore be readily self-administered. In the first of these studies involving 18
subjects, Bruce et al. compared the effectiveness of the Sea Band® acupressure band
with 0.6 mg of scopolamine, (hyoscine hydrobromide) and a placebo, to increase
tolerance to cross-coupled (Coriolis) stimulation. The subjects performed active
head movements on a rotating chair. The speed of the chair has been started at
1 rpm and every minute, increased by 1 rpm up to a maximum of 28 rpm. Each
subject was given three treatments, at least one week apart, namely: placebo drug
and placebo band; scopolamine and placebo band; placebo drug and active band.
The results have shown that the subjects’ tolerances to provocative motion were
significantly increased with scopolamine, but there was no such increase with the
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Sea Band® or the placebo. Bruce et al. suggested that the failure of the acupressure
bands to show any significant protection against motion sickness might be due to
insufficient movement at the wrist to provide adequate stimulation of the P6 point
by the plastic button of the band. Alternatively, they suggested that only a minority
of people would in fact show significant benefit, as noted with other experience
using medical acupressure. However, Bruce et al. have opined that transcutaneous
electrical nerve stimulation at the P6 point might be worth trying.
Warwick-Evans et al. (1991) used 36 male subjects, aged between 21 and
25 years (mean 21.3) in their double-blind placebo controlled study to evaluate the
effectiveness of Sea Band®, against motion sickness induced by Coriolis stimulation. Subjects were split into two equal groups, showing either high or low levels of
susceptibility to motion sickness, according to Reason’s Motion Sickness
Questionnaire (1975). Half of the subjects in each group used the acupressure band
and the other half the placebo. They found no significant difference, in terms of
protection against motion sickness, between the acupressure and placebo
conditions.
Electrical Acustimulation: In their study, Hu et al. (1992) decided to stimulate the
P6 point electrically in order to achieve greater response than has been possible
with conventional acupressure. They have done so by means of cutaneouis electrodes rather than needles and refer to this method as “electrical acustimulation.”
They planned two experiments to study the effects of electrical acustimulation on
both gastric myoelectric activity and the severity of motion sickness caused by
illusory self-motion in an optokinetic drum. First they have given 16 Chinese
subjects electrical acustimulation in one of two sessions. They found that both the
mean motion sickness symptomatology scores and tachyarrhythmia were significantly lower during periods of acustimulation than in those without. Second, they
randomly assigned 45 white and black American subjects into three groups, one of
which has received acustimulation, another sham acustimulation, and a control
group. Electrogastrograms and subjective evaluations of symptoms of motion
sickness were then obtained from each subject.
The mean motion sickness symptomatology scores in the acustimulation group
were found to be significantly lower than in the control group. That has not been the
case however, when the sham-stimulation group was compared with the control
group. Tachyarrhythmia in the acustimulation group was also significantly less than
in the control group, but not less than in the sham-stimulation group. Hu et al.
concluded that electrical acustimulation has reduced the severity of symptoms of
motion sickness and also appeared to diminish gastric tachyarrhythmia.
Relief Band®: Bertolucci and DiDario (1995) have also reported a study in which a
portable device, the Relief Band®, delivered acustimulation to the Neiguan
acupuncture (P6) point, in an attempt to control seasickness. They used 5 male and
4 female volunteer subjects, aged from 39–53 years, all of whom had a history of
motion sickness. The experiment was conducted on a 50-foot commercial boat
during three separate day trips on the open seas outside the San Francisco Bay. The
first trip lasted 5 h and the other two 11 h each. Subjects used the device either on
the P6 active point or on a placebo point. The subjects’ motion sickness symptoms
11.11
Other Methods Used to Treat Motion Sickness
243
were recorded prior to departure and then at hourly intervals for the first 3 h. These
symptoms have been graded as 1 (“feel fine,” no nausea or vomiting); 2 (slight
nausea); 3 (intermittent nausea but no vomiting); 4 (constant nausea, but no
vomiting) and 5 (intermittent vomiting, with or without nausea).
Bertolucci and DiDario found that 5 of the subjects with motion sickness who
had initially placed the device at the placebo site reported very little improvement in
their symptoms of motion sickness from a mean of 3.6 (±0.6, SD) to 3.4 (±1.1,
SD). On the other hand, the other 4 subjects who had initially used the device in the
P6 position reported a decrease in their symptoms from a mean of 4.3 (±1.0, SD) to
1.0 (±0.2, SD). The position of the Relief Band® was then switched to the placebo
position and their symptoms of motion sickness worsened from a level of
1.0 (±0.2, SD) to 4.0 (±1.4, SD). In the case of all of the 5 subjects on whom the
device had been moved from the placebo to the P6 position, however, their
symptoms of motion sickness had become significantly less going from a mean of
3.4 (±1.1, SD) to 1.0 (±0.7, SD). These researchers concluded that the severity of
motion sickness has been reduced by the use of portable acustimulation and that the
Relief Band® might be an effective alternative to the use of medications.
Miller and Muth (2004) have also examined the ability of both acupressure and
acustimulation as a means of preventing motion sickness during optokinetic drum
rotation. They concluded that, in their study: “Neither band nor placebo prevented
the development of motion sickness, regardless of whether the bands were used
correctly or incorrectly.”
Additional Methods: Barber (1976) has added that many other methods have been
used to control psycho-physiological functions, including hypnosis, autohypnosis,
autosuggestion, direct suggestion, meditation, and hatha yoga. He has also referred
to the use of autogenic training and relaxation, which techniques have already been
discussed.
11.12
Summary
• Due to the potentially dangerous side effects of motion sickness medications,
different forms of drug-free motion desensitization therapies have been
developed.
• In the early 1960s, I began a medication-free cognitive-behavioral desensitization programme for the Royal Air Force to help trainee fliers who suffered from
severe motion sickness. This programme was quite successful at utilizing both
cognitive and behavioral training to manage motion sickness symptoms.
• Since the middle of 1981, the RAF has drifted away from my original training
technique by including preconditions, detailed assessments, three forms of
provocative motion and remedial flying; the cognitive element of my programme has also been dropped.
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The Use of Non-pharmacological Therapy
• The United States Air Force and Navy as well as the Canadian Forces have all
used some form of desensitization, but unlike the RAF programmes, it usually
involves biofeedback.
• Other methods such as: acupuncture, acupressure, autogenic training, and
hypnosis have been used to combat symptoms of motion sickness, with mixed
results.
References
Aitken JR, Benson JW (1984) The use of relaxation/desensitization in treating anxiety associated
with flying. Aviat Space Environ Med 55(3):196–199
Bagshaw M, Stott JRR (1985) The desensitization of chronically motion sick aircrew in the Royal
Air Force. Aviat Space Environ Med 56:1144–1151
Banks RD, Salisbury DA, Ceresia PJ (1992) The Canadian forces airsickness rehabilitation
program. Aviat Space Environ Med 63:1098–1101
Barber TX (1976) Introduction. In: Barber TX et al (eds) Biofeedback and self-control. Aldine
Publishing Company, Chicago, IL
Benson JW, Aitken JR (1985) Psychological differences noted in aircrew members undergoing
systematic desensitization and their subsequent functioning. Aviat Space Environ Med
56:238–241
Bertolucci LE, DiDario B (1995) Efficacy of a portable acustimulation device in controlling
seasickness. Aviat Space Environ Med 66:1155–1158
Bower GH (1975) Cognitive psychology: An introduction. In W. K. Estes (ed.), Handbook of
learning and cognition (Pp. 25-80). Hillsdale, NJ: Erlbaum Associates
Bruce DG, Golding JF, Hockenhull N, Pethybridge RJ (1990) Acupressure and motion sickness.
Aviat Space Environ Med 61:361–365
Cowings PS (1990) Autogenic feedback training: a treatment for motion and space sickness. In:
Crampton GH (ed) motion and space sickness. CRC Press Inc., Boca Raton, FL
Cowings PS, Toscano WB, Kamiya J, Miller NE, Sharp JC (1988) Autogenic feedback training as
a preventive method for space adaptation syndrome on Space-Lab 3. Aviat Space Environ Med
59:481
Cowings PS, Naifeh KH, Toscano WB (1990) The stability of individual patterns of autonomic
responses to motion sickness stimulation. Aviat Space Environ Med 64:399–405
Dobie TG (1974) Airsickness in aircrew. AGARDOGRAPH No. 177, North Atlantic Treaty
Organization Advisory Group for Aerospace Research and Development, Neuilly-sur-Seine,
France
Dobie TG, May JG, Fisher WD, Elder ST, Kubitz KA (1987) A comparison of two methods of
training resistance to visually-induced motion sickness. Aviat Space Environ Med 58(9):A34–
A41
Dobie TG, May JG, Fisher WD, Bologna NB (1989) An evaluation of cognitive-behavioral
therapy for training resistance to visually-induced motion sickness. Aviat Space Environ Med
60:307–314
Dundee JW, Chestnutt WN, Ghaly RG, Lynas AGA (1986) Traditional Chinese acupuncture: a
potential useful antiemetic? BMJ 293:583–584
Dundee JW, Ghaly RG, Fitzpatrick KTJ, Lynch GA, Abram WP (1987) Acupuncture to prevent
cisplatin-associated vomiting. Lancet 1:1083
Dundee JW, Ghaly RG, Fitzpatrick KTJ, Abram WP, Lynch GA (1989) Acupuncture prophylaxis
of cancer chemotherapy-induced sickness. J R Soc Med 82:268–271
References
245
Giles DA, Lochridge GK (1985) Behavioral airsickness management program for student pilots.
Aviat Space Environ Med 56:991
Graybiel A, Knepton J (1972) Direction-specific adaptation effects acquired in a slow rotation
room. Aerosp Med 43(11):1179–1189
Graybiel A, Knepton J (1978a) Prevention of motion sickness in flight maneuvers, aided by
transfer of adaptation effects acquired in the laboratory: ten consecutive referrals. Aviat Space
Environ Med 49:914–919
Graybiel A, Knepton J (1978b) Bidirectional overadaptation achieved by executing leftward or
rightward head movements during unidirectional rotation. Aerosp Med 49(1):1–4
Graybiel A, Wood CD, Miller EF II, Cramer DB (1968) Diagnostic criteria for grading the severity
of acute motion sickness. Aerosp Med 39:453–455
Graybiel A, Dean FR, Colehour JK (1969) Prevention of overt motion sickness by incremental
exposure to otherwise highly stressful Coriolis accelerations. Aerosp Med 40:142–148
Hu S, Stern RM, Koch KL (1992) Electrical acustimulation relieves vection-induced motion
sickness. Gastroenterology 102(6):1854–1858
Jackson RJ (1994) A multimodal method for assessing and treating airsickness. Int J Aviat Psychol
4(1):85–96
Jacobson E (1938) Progressive relaxation. University of Chicago Press, Chicago
Jokerst MD, Gatto M, Fazio R, Stern RM, Koch KL (1999) Slow deep breathing prevents the
development of tachygastria and symptoms of motion sickness. Aviat Space Environ Med
70:1189–1192
Jones DR, Hartman BO (1984) Biofeedback treatment of airsickness: a review. In: Motion
sickness: mechanisms, prediction, prevention and treatment. AGARD Conference Proceedings
No. 372, AGARD-CP-372, North Atlantic Treaty Organization Advisory Group for Aerospace
Research and Development, Neuilly-sur-Seine, France, vol 42, pp 1–4
Jones DR, Levy RA, Gardner L, Marsh RW, Patterson JC (1985) Self-control of psychophysiologic response to motion stress: using biofeedback to treat airsickness. Aviat Space Environ
Med 56:11521157
Jozsvai EE, Pigeau RA (1996) The effect of autogenic training and biofeedback on motion
sickness tolerance. Aviat Space Environ Med 67:963–968
Lentz JM (1984) Laboratory tests of motion sickness susceptibility. In: Motion sickness:
mechanisms, prediction, prevention and treatment. AGARD Conference Proceedings No. 372,
North Atlantic Treaty Organization Advisory Group for Aerospace Research and
Development, Neuilly-sur-Seine, France, vol 29, pp 1–9
Levy RA, Jones DR, Carlson EH (1981) Biofeedback rehabilitation of airsick aircrew. Aviat Space
Environ Med 52(2):118–121
Li GX, Shi Q, Zhou JJ (1991) Application of bio-feedback relaxation and imagery exercises in
flight training. Aviat Space Environ Med 62:456
Miller KE, Muth ER (2004) Efficacy of acupressure and acustimulation bands for the prevention of
motion sickness. Aviat Space Environ Med 75:227–234
Spielberger C (1996) Theory and research on anxiety. In: Spielberger C (ed) Anxiety and
Behavior. Academic Press, New York, NY
Warwick-Evans LA, Masters IJ, Redstone SB (1991) A double-blind placebo controlled
evaluation of acupressure in the treatment of motion sickness. Aviat Space Environ Med
62:776–778
Wovters L, Amery W, Towse G (1983) Flunarizine in the treatment of vertigo. J Laryngol Otol
97:697–704
Chapter 12
Cognitive-Behavioural Desensitisation
Training—The Principles
of My Original Programme Using
a Rotating/Tilting Chair
Abstract When I devised the cognitive-behavioural desensitisation training programme some years ago, it was and still is based on the concept that chronic motion
sickness could well have both physiological and psychological features. My earlier
dismal experience with trying to identify successful predictors left me with the
feeling that in any given person, I was unable to decide whether his or her problem
with motion sickness was more physiological or more psychological. For those
reasons, I avoided the issue by planning to cater for both of these characteristics in
parallel, on the basis that each individual would get whatever quantum of each type
of help that was needed. I am bound to say that in retrospect, I could often have
made the correct judgment about the likelihood of success after the training was
completed. Does that really matter, however? I think not. You will make your own
decision on that point.
I conceived my programme of cognitive-behavioural desensitisation training for
alleviating motion sickness based on the premise that this malady is caused by a
physiological response to provocative motion stimuli, together with a varying
degree of psychological overlay (Dobie 1965, 1974). A person suffering from
severe motion sickness inevitably shows some degree of arousal or loss of confidence by the time he or she seeks help. This results in their firm personal belief that
he or she is particularly prone to motion sickness and there is little or nothing that
can be done about it other than avoiding that form of provocative motion, or taking
some form of medication. The cognitive-behavioural anti-motion sickness training
programme recognises this situation and is designed to deal with it. In this context,
it is interesting to note the following observation made by Wendt (1948): “It seems
not too much to hope that by an appropriate combination of psychological, physiological and physical procedures motion sickness can be reduced to the status of a
minor problem.” This is exactly what is involved in my cognitive-behavioural
desensitisation training programme.
The cognitive (counselling) component of the combined approach to the management of motion sickness plans to deal with that arousal problem or “anxiety
overlay.” It is important to stress, however, that this condition is not pathological
and never will be in my mind. It is a completely natural and quite understandable
protective response to a bodily discomfort in conditions of provocative motion and
© Springer Nature Switzerland AG 2019
T. G. Dobie, Motion Sickness, Springer Series on Naval Architecture,
Marine Engineering, Shipbuilding and Shipping 6,
https://doi.org/10.1007/978-3-319-97493-4_12
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Cognitive-Behavioural Desensitisation Training …
it is based on valid past personal experiences. By reducing this arousal, the subjects
can increase their amount of exposure to these potentially provocative stimuli that
they are able to endure, and habituate like others. They can then enter that motion
environment at levels that are further and further below their own motion sickness
(physiological) threshold, thereby permitting sufficient time for them to adapt to this
provocative motion. I shall address this issue further later. This adaptation also
boosts their confidence greatly and has a further positive effect on their ability to
withstand the effects of provocative motion that had caused their motion sickness.
The high arousal model of this malady suggests that there is little chance of
alleviating chronic motion sickness without intervention. For example, those people
who are prone to car sickness may ride in automobiles daily for many years without
apparent improvement, resulting in the inevitable belief that there is something
fundamentally wrong or different about them that causes them to be chronically car
sick. It is interesting to note that Charles Darwin reacted similarly during his
extended voyage on the Beagle. On June 3, 1836 he wrote, “… I positively suffer
more from sea-sickness now than three years ago” (Barlow 1946). The cognitive
(counselling) component of the combined approach to the management of motion
sickness sets out to deal with that arousal problem or “anxiety overlay.”
It is important, however, again to stress that this condition is not pathological. It
is a natural and understandable protective response to bodily discomfort in conditions of provocative motion and is based on valid past personal experiences. By
reducing this arousal, the subjects can increase the amount of exposure to these
potentially provocative stimuli, which they can endure, thereby habituating like
others. They can then enter that motion environment at levels that are further and
further below their own motion sickness (physiological) threshold, thereby permitting sufficient time for them to adapt to this provocative motion. I shall address
this issue further later. This also boosts their confidence greatly and has a further
positive effect on the ability to withstand the effects of provocative motion.
12.1
Cognitive-Behavioural Training—Historical
Perspective
The rest of this text will address, in some detail, my cognitive-behavioural programme for managing motion sickness. Perhaps it is not surprising that this is the
form of training that I favour because I feel that one should always treat the whole
person and not just one system within that person. In addition, this review of
managing motion sickness will give the reader a good insight into various aspects
of this malady. This overview includes my early results that have been obtained
with British Royal Air Force (RAF) flight trainees who had been permanently
grounded because of their apparently intractable airsickness and were the first to be
managed with this form of training. This will be followed by a review of our recent
experimental evidence carried out in the Psychology Department at the University
12.1
Cognitive-Behavioural Training—Historical Perspective
249
of New Orleans that supports the component parts of this training programme. After
that, various other desensitisation programmes will be compared and contrasted
with my cognitive-behavioural desensitisation training and the different features
will be highlighted. A unique feature of this report is that, unlike the others, my
results were not published until at least five years had elapsed after training ended.
The rationale of cognitive-behavioural training is based on the principle of
relieving the individual’s understandable state of anxiety by means of confidencebuilding briefings, while increasing adaptation to vestibular stimulation on a
rotating/tilting chair which provides a sensation that is frequently bizarre and disorienting (Dobie 1971). I first tested this programme of training to help student
flight trainees in the Royal Air Force (RAF) Flying Training Command who were
about to be withdrawn from flight training due to severe, apparently intractable,
airsickness. At that time only anti-motion sickness medications of various kinds
were then in use but, for safety reasons, these were restricted to dual-only flight
sorties because of side effects considered unacceptable for solo flying. Motion
sickness was causing the loss of significant amounts of flight training time and in
the worst cases, resulted in flight trainees being permanently grounded. Many
questions had arisen concerning the prevention and treatment of airsickness, but at
that time not many hard answers were available other than the restricted use of
anti-motion sickness drugs.
As I have already said earlier, when discussing airsickness, most flight trainees
who suffer airsickness when they first start flying usually adapt to the motion and
their symptoms disappear. This time scale varies with the trainees and also with the
format of the training programme and type of aircraft, since it depends largely on
the timing of provocative manoeuvres. In addition, some students have a long
history of airsickness and need more encouragement. However, there were others
who failed to respond to all help and reached the stage of becoming intractably
airsick. This becomes so severe that their instructors reach the highly costly and
undesirable stage of considering grounding them.
As a result of this undesirable event, the author decided to investigate the
possibility of helping these severely airsick individuals to return to flight training
successfully and eventually become useful, productive operational flight crew,
(Dobie 1974). This aim was achieved in a high proportion of cases. In time it also
became apparent that those, as who did recover finished above the average both
during flight training, and subsequently as operational aviators. We now turn to the
early days of this programme as a means of setting the scene. This includes a
discourse on the early results that were achieved among RAF flight trainees who
were successfully returned to flying after having been grounded because of
intractable airsickness.
I asked the Air Staff how long those flight trainees who had just been grounded
permanently with the diagnosis “intractable airsickness” could be made available to
me to give them a chance to overcome their chronic airsickness. After some consideration, I was advised that it would take about a month to decide what to do with
them now that they were grounded and I could have them for that length of time.
I jumped at that and agreed to take the next 50 trainees who were grounded and
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Cognitive-Behavioural Desensitisation Training …
give them a course of anti-motion sickness training, if the Air Staff would agree to
return them to the instructor at their flying training school for his evaluation of the
student’s ability to continue flying training without an airsickness problem; that was
all agreed. I fully realised that these trainees only had four weeks left in which to be
recovered as flight crew personnel, so it wouldn’t be ethical, or practical, to treat
some of them as a control group. So any way of evaluating the effectiveness of the
constituent parts of the training technique would have to wait for another day.
Having got that opportunity, I decided to tackle this problem by what is now
referred to as a “Cognitive-Behavioral Desensitisation Training Programme”. This
consisted of confidence-building counselling reinforced by means of vestibular
training to demonstrate the individual’s ability to adapt to provocative motion
(Dobie 1974). Flight trainees who suffer from severe incapacitating motion sickness
inevitably show some degree of anxiety or loss of confidence. This seems inevitable
because their future as aviators is in jeopardy. This suggests that vestibular training
alone is not enough; the anxiety overlay, or anticipatory arousal, as I prefer to call
it, also requires attention.
The rationale of cognitive-behavioural training is based on relieving an individual’s anticipatory arousal while building acclimatisation to vestibular stimulation
on a rotating/tilting chair. The passive whole bodily movements produce
cross-coupled (Coriolis) stimulation of the semicircular canals resulting in a sensation that is frequently bizarre and disorienting. The stimuli are carefully controlled so that no subject ever experiences more than the earliest (threshold)
symptoms of motion sickness and no one has ever been close to emesis. This is
critical to the development of renewed confidence. The technique addresses the
individual’s main problems in parallel, namely, a heightened state of arousal
together with a lack of acclimatisation to motion. The candidate’s improved performance on the rotating/tilting table, shown by an ability to withstand increasing
amounts of vestibular stimulation over time, depends greatly upon the counsellor’s
handling of the subject and increases confidence and lessens arousal.
Although my cognitive-behavioural training programme was originally designed
to overcome airsickness, the principles involved are effective in dealing with all
forms of motion sickness. representation of Dobie and May’s psycho-physiological
model of motion sickness, based on Benson’s purely physiological model (1988),
together with our added psychological cognitive factors (shaded area) are all shown
in Fig. 12.1 (Dobie et al. 1989).
In all cases, the management was similar: a flight trainee who had been grounded
on the basis of intractable airsickness was referred to my office so that he was
removed from his local environment. (At that time all flight trainees were male.)
The main purpose of the initial consultation, lasting just over one hour was
designed to establish in the mind of the trainee that airsickness during flight training
was both common and “normal”. The ability to identify with normality is considered to be the first and most important step to recovery.
I had already asked the trainee to bring to the interview any documents relevant
to his flying and medical status, including a detailed history of his airsickness.
These documents were left on my desk, obviously unopened, for the greater part of
12.1
Cognitive-Behavioural Training—Historical Perspective
251
Fig. 12.1 A schematic of Dobie and May’s psychophysiological model of motion sickness based
on Benson’s physiological model
the initial interview. I intended this to convey the notion that I was discussing
airsickness in general and not a condition peculiar to the individual. However, by
the end of this discussion I hoped to have covered in general terms all aspects of the
subject’s motion sickness problems. I placed great emphasis on the fact that airsickness was common and could be overcome. It was noticeable that during this
initial discussion the person became more talkative and showed signs of becoming
more relaxed as time went on. I then described the principles of my
cognitive-behavioural desensitisation training and asked the subject if he wished to
enter the training programme. The subject was assured that his agreement to do so
did not imply a commitment on his part to return to flight training and that such a
return was contingent upon the subject feeling well enough, and wishing to do so.
I pointed out that some trainees, consciously or subconsciously might simply
dislike military flying and then asked him if he wished to reconsider military flying
as a career. This allowed the subject to have a change of heart and give me an
opportunity to assess the individual’s keenness to fly. Whatever the outcome, no
one was excluded from the programme, as a result of my initial evaluation; that was
merely recorded confidentially for later review at the end of the training. It was
emphasised that anyone could opt out of the programme at any time. I adopted this
attitude while the subject was anxious and under-confident, so that he did not feel
trapped into a long term commitment before seeing a chance of success.
The first 50 unselected cases referred to me all decided to proceed with the
training as described, some with greater alacrity than others. Notes made at the time
showed that those few trainees who demonstrated less enthusiasm than others at the
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Cognitive-Behavioural Desensitisation Training …
prospect of proceeding, subsequently failed. One could not rely on these observations as firm predictors at such an early stage, however, but could be called upon
later if a particular person failed to make progress, as had been expected.
Having completed the initial interview in my office and gained the approval of
the trainee to start the cognitive-behavioural training, arrangements were made to
meet again as soon as possible where my training equipment had been installed.
The rotating/tilting chair was built to my specifications at RAF St. Athan; it produced passive cross-coupled (Coriolis) vestibular stimulation. The subject’s chair
could be tilted through 90° in the fore and aft and lateral planes, or any combination
of these two manoeuvres at the same time, while the turntable on which the chair
was mounted was being rotated in either direction. The maximum rotational speed
of the chair was 20 rpm. The severity of vestibular stimulation which could be
imposed by this type of equipment depended upon three variables; the speed of the
rotating platform, the pattern of the tilting manoeuvres and the number of these
manoeuvres which were carried out during a single training session. A photograph
of the original RAF chair is shown in Fig. 12.2. The subject was supplied with an
abort switch to end the run at any time, if he wished to do so for any reason.
In the early stages of the programme, I planned exposures to various motion
patterns in order to increase an individual’s level of adaptation to vestibular Coriolis
acceleration without producing an uncomfortable degree of motion sickness. Since
the main objective of the training was to increase confidence, it was critically
Fig. 12.2 Original RAF rotating/tilting turntable
12.1
Cognitive-Behavioural Training—Historical Perspective
253
important to limit the severity of exposure to provocative motion to a level that was
within the subject’s current capability. A severe bout of motion sickness during a
session could well have the reverse effect. At no time has any subject vomited while
undergoing motion desensitisation on the turntable.
12.2
Rationale of Cognitive-Behavioural Training
In this form of training the adviser focuses on the psychological aspects of stress
management and endeavours to instill a belief that the individual can indeed tolerate
noxious or stressful situations. As previously explained, once this idea has been
established, it is reinforced by means of controlled exposures to non-specific
provocative motion stimuli. In the early days of this programme I had used
cross-coupled (Coriolis) stimulation. More recently, the programme has included
illusory motion as a provocative stimulus; (that is in the subject of Chap. 13 of this
book, when I discuss using illusory motion in an optokinetic drum, instead of this
rotating–tilting chair). While the technique appears to involve habituation and
adaptation to a particular situation, our controlled studies have shown that mere
repetitive exposure without counselling has proven not to be beneficial in protecting
subjects against provocative motion (Dobie 1989). A key element in the technique
concerns the individual’s ability to learn to control the focus of cognitive processes.
This is an important part of the training so it is important that emphasis is always
placed on the normality of this protective response to provocative situations.
The main difference in individual susceptibility to motion sickness for a given
provocative motion profile could be physiological. However, I consider that it is
more likely that these differences are due to personal experiences in these environments and how the individuals react to them, as depicted on the schematic model
of motion sickness previously shown in Fig. 12.1. Those variables include practice,
attitude of mind, levels of mental arousal, and so on. It has long been reported that
passengers have been known to indicate that they feel sick before the ship leaves
the dock (DePuy 1896). On the other hand, there are those who claim that they
never get seasick, however rough the sea may be, whereas these same individuals
may state that they cannot cope with other forms of provocative motion, such as
fairground devices. There are indeed many seeming anomalies in individual histories of motion sickness. This tends to support the notion that there is more to this
problem than a physiological explanation alone. Perhaps these different individual
responses to provocative motion are determined by where an individual lies along
the underlying causative psycho-physiological spectrum. This will vary from person to person and vehicle to vehicle (or stimulus to stimulus), as attitudes differ and
the amount of anticipatory arousal varies.
In my opinion, the main difference between an individual who is apparently
sensitive to motion and one who is seemingly not, is mostly a feature of the arousal
that is created by exposure to a particular provocative motion environment. The
so-called “resistant” individual enters that environment with zero arousal and can
254
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Cognitive-Behavioural Desensitisation Training …
cope with a considerable amount of provocative stimulation before reaching his or
her threshold of response (i.e. beginning to feel motion sick). At the same time,
these relatively lengthy exposures to provocative motion allow time for adaptation
to take place. In that situation, a purely “physiological” model of motion sickness is
at work. However, the matter is quite different for people who have a history of
motion sickness. These individuals enter a provocative motion environment with a
varying degree of arousal dependent upon their previous motion experiences,
particularly if these exposures have caused motion sickness. Why is it, you may
ask, that these individuals seem to be different in the first place? Perhaps it is a
reflection of how an individual is first introduced to provocative motion. I suggest
that, depending upon the frequency and severity of that introduction, an individual
may either become sensitised or adapted to the motion environment.
Permit me to clarify this observation. The contents of Table 12.1 are by no
means exhaustive, but merely serve to indicate what I have mind. For example, if
early exposure to provocative motion is concerned with a child’s family visits by
automobile, it is clear that these experiences can vary significantly in terms of their
motion responses. Regarding the seven elements listed in the two columns of
Table 12.1: going once or twice a week is better than once a month; short trips
initially aid adaptation, whereas long ones may lead to motion sickness. Are you
riding in a vehicle with a stiff suspension that keeps you out of the range of motion
that is most provocative, or are you exposed to a lower, more provocative frequency
of motion? In some forms of “vehicular” motion, the person may have some means
of control, which is more protective than no control. Children in the back of a
vehicle, who cannot see much looking forward and/or are playing with siblings, are
likely to perform more head movements that add to the quantum of stimulus. Focus
of attention is more protective and conducive to permitting adaptation through
cognitive processing; bearing in mind that reading can be counter-productive.
Finally, starting off feeling sick can lead to sickness that may be incorrectly labeled
as “motion sickness”, so that mislabeling can often occur and be interpreted as
super-sensitivity to the effect of provocative motion. You can visualise parallel
scenarios for all forms of provocative motion, whether it is a student aviator’s
introduction to flying or a would-be sailor’s introduction to sailing. You will note
that these various factors have been discussed throughout this book.
Table 12.1 Aids to adaptation during early introduction to provocative motion
Facilitates adaptation
Frequent exposures
Short duration
Low provocative motion characteristics
initially
Subject controls device
Minimal added head movements
Subject’s attention focused
Good general state of health
Encourages sensitization
Infrequent exposures
Long duration
High provocative motion characteristics
initially
No control over device
Excessive added head movements
Minimal focus of attention
Not feeling too well
12.2
Rationale of Cognitive-Behavioural Training
255
In other words, the degree of arousal can vary with the different types of
provocative motion, based on experiential expectations. This is the effect of the
psychological component that is added to the basic sensory conflict, or whatever,
(physiological) model of motion sickness. The subject gets closer to the onset of
motion sickness (threshold of response) in a shorter time, depending on the degree of
arousal. In the more severe cases, this can occur on entering (or even before entering)
the provocative motion environment. This also means that each exposure to
provocative motion will be relatively short before the onset of motion sickness, and
consequently there is little time to adapt. This concept is portrayed in Fig. 12.3. It
should be stressed that individuals vary in their states of arousal depending upon the
particular form of provocative motion. In other words, an individual may approach
one type of provocative stimulus with minimal arousal whereas that same person
may well generate the opposite response to another form of provocative motion. This
represents a reaction to the individual’s past experience with different types of
potentially provocative stimulation and dictates whether or not an individual feels
comfortable in a particular situation. In terms of the model depicted in Fig. 12.3, not
only do individuals vary from others, they can also vary within themselves in their
state of arousal prior to entering different types of provocative motion.
Fig. 12.3 Dobie’s psychophysiological concept of motion sensitivity
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Cognitive-Behavioural Desensitisation Training …
Figure 12.3 represents the conceptual difference between a purely physiological
model of the aetiology of motion sickness and my psychophysiological approach
that introduces the view that anticipatory arousal can interfere with adaptation to
provocative motion.
In the purely physiological concept, represented by the first two columns, it
suggests that a person who is motion sensitive (MSS) has a very low tolerance to
provocative motion compared to another individual (column 2) who is apparently
motion resistant (MRS).
In my view, however, there is no fundamental difference in the amount of
provocative motion that these types of people should be able to withstand. In other
words, I believe that all individuals have roughly the same (physiological) threshold
to provocative motion, given the opportunity to achieve it. However the anticipatory arousal that affects those in columns 4 and 5 does not allow them to remain in a
provocative environment long enough to adapt and achieve that potential. This is
characterised by the three columns under the psycho-physiological heading that
suggest a difference based on individual anticipatory arousal prior to the onset of
provocative motion. A person with minimal arousal (A) in column 3 should be able
to adapt to motion in a fashion similar to the apparently resistant individual in
column 2, because both individuals are exposed to roughly the same amount of
motion, which gives time for adaptation to occur. As the amount of arousal
(A) increases, however, the persons represented by the fourth and fifth columns are
increasingly closer to sickness at the onset of motion. The person in the fifth column
doesn’t have the opportunity to adapt. A reduction in arousal is then needed before
those in columns 4 and 5 can withstand a longer period of exposure to provocative
motion without experiencing adverse responses; thereby allowing adaptation to
occur.
Cognitive-behavioural training has been developed to overcome these
psycho-physiological effects produced by provocative motion stimuli that cause a
person to become motion sick. I believe that by dealing with both the physiological
and psychological components at the same time, it does not matter which of these
features is the more dominant in any individual. Physiological differences between
individuals may exist, but are difficult to quantify or characterise. For the purposes
of training, however, it is not beneficial to focus on the possibility that one individual is physiologically more prone to motion sickness than another. Indeed, the
subjects’ belief that they are physiologically different from those whom they perceive to be resistant to motion stimuli is in itself part of the psychological overlay.
As the training reduces the person’s anticipatory arousal he or she soon begins to
react to provocative motion like those other individuals who have apparently
seemed to be resistant.
As we shall see, the training patterns of the fifty subjects and their results gave a
good indication of the ultimate outcome in the majority of cases; the small group
whose training was unsuccessful exhibited characteristic features. Their progress
was erratic and the development of adaptation was found to be limited in those
subjects who seemed to lack enthusiasm for flying and who prevaricated in
response to direct questioning about accepting training. For this reason, the
12.2
Rationale of Cognitive-Behavioural Training
257
programme can be used as a combined “evaluation/training technique” (Dobie
1971); it should be stressed that a 10% failure rate at that stage of training was
significantly lower than usual (Dobie 1974). This seemed to indicate that the trainees who were treated for intractable airsickness were above average students. That
conclusion was supported by a long-term follow-up which took place some six or
more years later, by which time the candidates had been flying on operational
squadrons for a number of years. The follow-up confirmed the successful retention
of all of our ex-subjects who had completed training. In addition, this group of
individuals was rated above the average. It also confirmed that they were no longer
hampered by motion sickness; we shall see later that is a key issue.
When I first began this cognitive-behavioural desensitisation training programme in the RAF, the desensitisation part of the procedure was carried out by
means of cross-coupled (Coriolis) stimulation using a rotating/tilting chair designed
to provide passive vestibular stimulation (see Fig. 12.2). The subject, head
restrained, was strapped into his seat and supplied with an abort switch. The
turntable could be rotated in either direction at controlled rates up to 20 rpm. In
addition, the subject’s chair, located on top of the turntable, could be tilted ±50°
either in the fore and aft or lateral planes, or both at the same time. When all three
were operated together—namely, rotation and both tilting planes; this provided
passive cross-coupled (Coriolis) vestibular stimulation. These positions of subjects
undergoing training on the rotating/tilting chair, that are shown in Fig. 12.4, are the
limits of tilt that were built into the design of the apparatus, which does not mean
that maximum tilts were used all the time; in the early runs it was usual to use
restricted tilting manoeuvres to minimise the tilts diagrammatically in the following
Fig. 12.4.
The stimuli were carefully controlled so that the individual never experienced
more than the early symptoms of motion sickness, and no one ever came even close
to emesis. I firmly believed, and still do, that this aspect of the cognitivebehavioural approach was critical in order to develop a subject’s confidence. In
other words, this technique was designed to address, in parallel, the main problems
that caused motion sickness, namely, a lack of acclimatisation to provocative
motion and a state of heightened arousal associated with a particular form of motion
or motions. When a candidate improved his performance on the rotating/tilting
table, as shown by his ability to withstand increasing amounts of vestibular stimulation over time, this also helped to increase his confidence and lessen the arousal.
Although this form of training was originally designed to treat airsickness, the
principles involved are appropriate to managing any form of motion sickness.
I always made it clear to subjects that they were not being trained to cope with the
particular type of provocative motion provided by the desensitisation device. That
was only a convenient means to an end. The device was merely being used to
induce a motion sickness response and the purpose of the programme was to teach a
person how to cope with that response, no matter how it had been caused. In that
sense, the “response” was being used as the desensitisation stimulus. I should stress
that this behavioural training was always accompanied by cognitive stressor
management; behavioural training never occurred alone.
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Fig. 12.4 Various tilt patterns on the rotating/tilting chair, shown diagrammatically, as seen from
above
I had elected to take the next 50 persons who had been grounded with a diagnosis of intractable airsickness and gave them a course of cognitive-behavioural
anti-motion sickness training. No form of pre-selection was involved. These results
will be shown later in Table 12.2. Only 7 subjects (14%) failed subsequently
because of recurring airsickness, giving a success rate of 86%. It is important to
note that this success rate was arrived at after a long-term evaluation of current
success; at least five years after the clients had been returned to flight training, so
that it also included post-graduate squadron experience. These results will be discussed in more detail when I compare them with the results of other military
programmes.
The training patterns of the first fifty unselected subjects, who had been
grounded with intractable airsickness and entered my programme, had given a good
indication of the ultimate outcome in the majority of cases. Those who turned out to
be successful candidates had shown a good response in terms of adapting to
incremental increases in vestibular stimulation together with increasing enthusiasm
to complete their course of training and return to flying. On the other hand, the
12.2
Rationale of Cognitive-Behavioural Training
259
Table 12.2 Dobie’s results five years after cognitive-behavioural desensitisation training
Class
Total
Pass
Fail
Not airsick
Airsick
6b
Student aircrew
44
34
4a
e
c
Qualified aircrew
6
4
1
1d
All
50
38 (86%)
5
7
a
3 failed because of poor airwork and 1 left the Service for family reasons. None of these suffered
from airsickness
b
2 admitted that they had begun to dislike flying prior to being exposed to any violent aerobatic
maneuvers or suffering from any symptoms of airsickness
c
Failed because of poor airwork—no signs or symptoms of airsickness
d
Marked phobic element in this case
e
2 of these cases showed evidence of phobia related to a particular aircraft type
small group of subjects whose training had been unsuccessful exhibited characteristic features. Their progress had been erratic and the development of adaptation
had been limited in those subjects who had seemed to lack enthusiasm for flying
and who had prevaricated in their response to direct questioning about their desire
to accept preventive training. However, in these early stages of developing and
testing the cognitive-behavioural training programme it was too soon to act on these
pointers. For this reason, the programme could be considered for use as a combined
evaluation/treatment use (Dobie 1974) at a later stage.
12.3
Practical Application Using the Rotating
Tilting Chair
The cognitive-behavioural training programme consisted of an initial briefing followed by a number of training sessions that include practice in a provocative
motion environment. The counselling component is an intrinsic part of the whole
procedure, at every step. This chapter merely provides a brief overview of the
programme. Those planning to carry out this technique are recommended to obtain
a copy of the “Handbook of Cognitive-Behavioural Anti-Motion Sickness
Training,” which is being prepared for would-be training advisers.
Initial Briefing The initial briefing consists of giving the subject an overview of
motion sickness in general, its causes, frequency and widely varying individual
responses. The aims, in summary, are as follows:
• Establish the normality of the motion sickness response to certain types of
motion stimuli.
• Emphasise that this is not a neurotic response, but a protective response.
• Emphasise that it is very common; to be incapable of exhibiting a motion
response would be abnormal.
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• Point out that the terms motion sickness and motion illness are really misnomers. The person is not ill, but exhibits the signs and symptoms of a disorder
due to the protective response. The only abnormal feature present is the motion
environment.
• Having emphasised the normality of this response to provocative motion,
explain that the term motion sickness continues to be used because, regrettably,
it has become the accepted term.
• Describe the background, previous experiences, and results that have arrived at
the present state of knowledge and the reasons for using cognitive-behavioural
training in the management of motion sickness.
• Aim to discuss the subject of motion sickness in general principles and avoid
personalising this condition. This is intended to encourage the subject to
understand that his or her motion history is not unique after all. This helps the
individual to reestablish his or her confidence, which is the first step on the road
to recovery.
• Inform subjects that during ensuing training sessions it will then be appropriate
to focus on their personal past experiences with motion stimuli and on their
current success in dealing with a provocative motion environment. While they
are being exposed to brief periods of provocative motion, they will be taught to
focus on exocentric problems and events of interest. Distraction caused by
conversing on subjects of interest can readily take their mind of stressors. They
will also be told (and this is the most important point) that these motion
exposures would always be carried out at or below their threshold for motion
sickness. This will reinforce the attitude that they can successfully cope with
motion stimuli.
Although this initial briefing lasts about an hour, it may extend longer if that
seems appropriate. The scene is being set for the subject by describing what is
known about motion sickness, and the emphasis is placed on the normality of the
motion response. The adviser discusses early experiences with the management of
the condition, as previously described under “Cognitive-Behavioural Training–
Historical Perspective.” The session builds to a logical conclusion by describing the
reasons for adopting the cognitive-behavioural management approach and ends by
describing that programme briefly and offering the subject the opportunity to participate. At this stage, the adviser continues to avoid specific reference to the
subject’s own motion sickness symptoms and experiences.
Training Sessions After obtaining the subject’s consent to continue the programme, the plan is to start the initial training session by obtaining information
about the subject’s prior motion experiences and reactions. Hopefully most, if not
all, of these types of situations will have been covered during the initial briefing,
since they are common responses that affect many people. The fact that most will
have been discussed already helps to convince the subject that these are indeed
common and not specific to them. This can be reassuring and provide a sense of
hope for future success.
12.3
Practical Application Using the Rotating Tilting Chair
261
The main concern in the behavioural component of this training is to expose the
subject to a provocative motion environment in a controlled fashion. These controlled exposures help to desensitise the subject and at the same time boost confidence. In the first training session, the adviser and client together must determine
the length of time that the client can tolerate the selected provocative stimulus
before experiencing the first early signs or symptoms of motion sickness. This is
termed the threshold of the motion sickness response on whatever device is to be
used for reinforcement training. In this programme, the desensitising element may
be provided by either cross-coupled (Coriolis) stimulation or visually-induced
apparent motion. The former may have some advantages over illusory motion, but
not always.
My basic philosophy is not to exceed a subject’s threshold of response, because
to do so is counterproductive and likely to reinforce an individual’s belief that they
are indeed hypersensitive to provocative motion. During the first session, the
adviser aims to identify the duration of stimulation that represents a subject’s
threshold. In the second session the level of that threshold of response is confirmed.
The adviser is ready to reduce the planned duration of that exposure, if necessary, to
prevent uncomfortable motion sickness responses, because some clients may have
experienced discomfort after the end of the first session. If necessary, the adviser
may also decrease the duration of exposure during the third session to ensure a
successful outcome. Later sessions deal more particularly with the idiosyncratic
responses of the individual, and the confidence-building discussions and duration of
reinforcement training are tailored accordingly. The adviser will then increment the
exposure durations carefully as the subject adjusts to the provocative stimulus.
Golding and Stott (1995) have carried out an interesting study to evaluate the
possible effects of varying the predetermined malaise level at which provocative
motion challenges are stopped, on the rate of habituation to these stimuli. The main
aim of their investigation has been to determine if the rate of habituation would be
affected by reducing the malaise level goal of each exposure, from moderate nausea
to mild symptoms (no nausea). A secondary aim has been to see if some of the
symptoms of motion sickness habituate more quickly than others.
In terms of habituation, the most robust observation that they have made has
been that the subject’s ability to tolerate the motion challenge to any particular
sickness rating increases with the number of provocative sessions. Golding and
Stott suggested that, within the range studied, habituation merely seems to increase
with the number of motion challenge sessions rather than the variation of malaise
level. They have then altered their desensitisation protocol to reduce the proportion
of motion challenges causing overt nausea. This has shortened the recovery time,
and as a consequence, has permitted more motion challenges to be completed per
day. They have opined that this should lead to quicker progress.
Golding and Stott also noted that reducing the proportion of sessions that continued to high levels of malaise might benefit some people. They have previously
noticed by chance that one of their subjects, who had great difficulty in habituating
to provocative motion, improved dramatically when the challenges had been kept to
a level that caused only mild symptoms of motion sickness within each exposure,
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despite the fact that his overall exposure to motion had been reduced. This led them
to conclude that in a small number of individuals repeated exposure to high sickness levels might result in sensitisation to provocative stimulation rather than
desensitisation. These findings support the general strategy that I had adopted from
the very beginning of designing the cognitive-behavioural training programme.
The cognitive or counselling component of the cognitive-behavioural training
sessions deals with the predictable arousal problem, or “anxiety overlay,” commonly associated with provocative motion environments. I stress that by reducing
this arousal clients can increase the amount of exposure to provocative stimuli,
thereby habituating as others have done. In order to help them during the initial
sessions, subjects are encouraged to focus their attention on a complex mental task,
which is suggested to them. For example, mental arithmetic is usually more
effective as a means of focusing attention than mere conversation, which requires
much less mental effort, unless the client becomes deeply involved in the subject.
As the clients begin to win the mental battle and ignore these provocative
stimuli, the need for artificial strategies to focus attention diminishes. This occurs
quite rapidly as their confidence builds. The subjects begin to relax physically and
their exposure times rise much more quickly as they begin to habituate to the
environment. There are individual differences in the rapidity of this improvement,
depending upon the severity of the motion sickness history and, no doubt, also as a
feature of personality variables.
The remaining training sessions give the subjects increasing confidence as their
exposure times to provocative motion increase and feelings of motion discomfort
decrease or disappear altogether. In these later training sessions, I introduce random
changes to the basic controlled stimulation, such as altering the speed and/or
direction of rotation of the device, or changing illumination. The total number of
training sessions should extend over a period of three or four weeks. This allows
time for the information to be absorbed and for the individual’s confidence to grow.
In addition, by performing the training over a number of weeks, the subject has the
opportunity to practice these techniques in the real world as well as on the training
device.
The rotation of the turntable and the tilting of the chair are both controlled
remotely from the turntable by means of a computer at the operator’s control panel
which is equipped with a means of measuring the duration of stimulation selected
by the counsellor. The NBDL software in the computer controls all of these features
and allows the operator to control the duration and pattern of individual training
profiles. On the other hand the subject is not left out of the picture; he or she can
switch off the system at any time, for any reason, by means of an abort switch
which he or she holds in the hand throughout the run. In addition, the subject is also
in auditory communication with the counsellor at all times.
The counsellor plans exposures to various motion patterns in order to increase an
individual’s level of adaptation to vestibular Coriolis acceleration without producing an uncomfortable degree of motion sickness. Since the main objective of the
training is to increase confidence, it is critically important to limit the severity of
12.3
Practical Application Using the Rotating Tilting Chair
263
exposure to provocative motion. A severe bout of motion sickness during a session
could well have the reverse effect.
In order to ensure that a subject does not experience symptoms of motion
sickness during the earliest sessions, the counsellor identifies and confirms each
subject’s threshold of response to provocative motion during the first two training
exposures. This threshold is considered to be the onset of the subject’s motion
sickness response and no more. Later sessions are tailored to the individual subject
according to his or her progress and level of adaptation. The various patterns of
tilting, producing different degrees of stimulation, have been shown earlier. The
subject is informed that this form of training is not a “trial of strength”. This is
intended to ensure that he or she does not exceed the personal threshold of
response.
During the early sessions, it is recommended that square patterns only are used
and at a rotational rate of 10 rpm. The direction of rotation of the turntable should
be varied, however on an ABBA pattern. This gives the counselor more control at a
stage when the subject is particularly vulnerable, because by so doing the only
variable is the duration of exposure. If different stimulus patterns are used during
these early stages (other than rotational direction), it is difficult to assess the different levels of stimulation for different patterns. At later stages, however, both
patterns of motion and rates of rotation can and should be varied in order to avoid
specificity of adaptation.
Each subject is given one or two, or even three training sessions per day but the
subsequent run or runs are always cancelled if any aspects of the residual motion
sickness remain from the previous session. The vestibular training pattern and
magnitude of vestibular stimulation on a given session are adjusted according to the
severity of symptoms produced by the previous session. The programme is aimed at
increasing a subject’s exposure to vestibular cross-coupled (Coriolis) acceleration
as much as possible without producing an unacceptable degree of motion sickness.
As already described, subjects are asked to maintain a personal graph of their
pattern of treatment in order to emphasize their progress. It is particularly important
that the counsellor does not become the subject’s “prop”; otherwise this form of
training would be open to much of the criticism levelled at the pharmacological
approach where subjects lean heavily on the availability of their medication.
The duration of the training programme is tailored to the level of the individual’s
responses to the stimulation. Although there is no critical end-point in terms of
stimulus intensity, one tries to achieve sufficient adaptation that the subject can
sustain random tilt patterns at a speed of rotation of 90°/s without significant motion
discomfort. In successful cases, this usually takes about three weeks. When subjects
are clearly coping well with this level of vestibular stimulation, the counsellor asks
them to indicate when they are ready to return to their own adverse motion
provocative environment. If they show confidence and keenness in reply, the
counsellor arranges for them to do so. As was the case in the original RAF programme, there is no formal follow-up procedure, since this lack of follow-up
suggests that the counsellor is confident that the subject needs no further supervision and can now cope with provocative motion.
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After obtaining the subject’s consent to continue the programme, we start the
initial training session by obtaining information about the subject’s own motion
experiences and reactions. Hopefully most, if not all, of these will have been
covered during the initial briefing since they are common to many people. The fact
that most will have been discussed already helps to convince the subject that these
are indeed common responses which affect many people.
The main concern in the behavioural component of this training is to expose the
subject to a provocative motion environment in a controlled fashion. In the first
training session after the initial briefing, the counsellor and client must determine
the length of time that the client can tolerate the selected provocative stimulus prior
to experiencing the first signs or symptoms of motion sickness. This is termed the
threshold of the motion sickness response to the cross-coupled (Coriolis) stimulation on the NBDL rotating/tilting chair. This threshold has to be obtained very
carefully to avoid the subject experiencing the stimulation too long and becoming
sick.
My basic philosophy is not to exceed a subject’s threshold of response to
provocative motion in the first few training sessions. During the first session, the
counselor should aim to identify the duration of stimulation which represents that
threshold. In the second session he should try to confirm that threshold and stop
there; indeed the counselor should be ready to reduce the planned duration of
exposure if necessary, in order to prevent uncomfortable motion sickness responses.
In that event and, if necessary, the counsellor should decrease the duration of
exposure during the third session, to ensure a successful outcome. Later sessions
deal more particularly with the idiosyncratic responses of the individual, so that the
counselor tailors the confidence building discussions and duration of reinforcement
training accordingly. He then increments the exposure durations carefully, as the
subject adjusts to the stimulus; it is useful to be able to get the client involved in
talking about a subject that interests him near the end of the planned duration, since
it distracts him and suppresses responses.
The cognitive or counselling component of the cognitive-behavioral training
sessions deals with the predictable arousal problem commonly associated with
provocative motion environments. The counselor stresses that by reducing this
arousal, clients can increase the amount of exposure to provocative stimuli, thereby
habituating as others have done. In order to help them during the initial sessions, the
counsellor encourages them to focus their attention on a complex mental task,
which he suggests to them, such as counting backwards by threes or reciting the
alphabet backwards. The more complex the problem, the more protective it is. For
example, for some, mental arithmetic is more effective in focusing attention than
mere conversation, which requires much less mental effort. This does not mean that
subjects will need to use such tricks in the long term. The purpose of this strategy is
merely to help them to ignore the stimulus in the early stages of training and be able
to relax physically in the provocative situation. It is important to stress the distinction between mental and physical relaxation. It is important that subjects
achieve a high level of mental focus in order to block out their motion responses.
Increased physical relaxation, on the other hand, is a useful indication that the
12.3
Practical Application Using the Rotating Tilting Chair
265
person’s level of arousal is coming under control; that can be done by getting him to
‘wiggle’ his jaw during the early session to check the tension, just as he is trained to
do at the start.
As the clients begin to win the mental battle and ignore these provocative
stimuli, the need for artificial strategies to focus attention diminishes. This occurs
quite rapidly as their confidence builds. They then begin to relax physically and
their exposure times rise much more quickly, as they begin to habituate to the
environment. There are individual differences in the rapidity of this improvement,
depending upon the severity of the motion sickness history and, no doubt, also as a
feature of the subject’s own personality.
The remaining training sessions give the subjects growing confidence as their
exposure times to provocative motion increase and feelings of motion discomfort
decrease or disappear altogether. In these later training sessions, the counsellor
makes random changes to the basic controlled stimulation. In the case of Coriolis
stimulation, he varies the pattern and direction of movement of the rotating/tilting
chair and the speed of rotation of the platform. He also turns the room lights off and
on at random and without warning; he also makes an excuse to leave the room for a
few moments while the training device is still running; for the sake of safety,
however, he keeps an eye on the turntable from outside the room.
The total number of training sessions should extend over a period of three or four
weeks. This allows time for the information to be absorbed and for confidence to
grow. In addition, by performing the training over a number of weeks, the subject
has the opportunity to practice these techniques in the real world as well as on the
training device. The following information is intended to give counsellors some
ideas on how to proceed during the training sessions. It should be pointed out,
however, that these are only samples. After the first two training sessions the
remaining sessions will vary with individual progress. In other words, counselors
will work around the subsequent numbered sessions until ready to proceed to the
next (e.g., session type 3, then session type 4, etc.).
12.4
First Training Session
The major aim of the first training session is to establish the individual’s threshold of
motion sickness response on the training device.
Like all subsequent training sessions, the counselor begins the first session by
asking if the subject has any questions or comments concerning the previous session. Whereas the initial briefing was predominantly a discourse by the counselor,
during the training sessions the aim is to encourage the subject to lead and the
counselor to act as an informed sounding board. In this session, the counselor
clarifies any queries the subject may have about the theory that has been presented
during the initial briefing session and takes every opportunity to be positive and
encouraging when discussing previous results and experiences with the trainee.
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He then reviews the subject’s personal motion history, written or verbal, as the
case may be, pointing out that this is the first time that he is aware of these details.
This is meant to reinforce the fact that what was said during the initial briefing was
general, and applied to all. The history review can often reveal useful information,
which should be related to that initial briefing. In other words, the subject’s personal
motion sickness history should be shown to be a common and absolutely normal
response to an abnormal situation. This is an opportunity to explain that the subject
may have been unlucky in the frequency and duration of early exposures to
provocative motion. Factors may have tended to sensitize him or her to motion
rather than enhance habituation, as would have been the case if circumstances had
been different.
Now is the time to establish the subject’s threshold of motion sickness response
to the rotating/tilting chair being used for reinforcement training. The counselor
briefs the subject carefully to ensure that the end-point of this evaluation is the
ONSET of motion sickness. He stresses that as soon as the first recognisable
symptoms of motion sickness appear, the subject should indicate this. At that point,
the counselor stops the device. Subjects are advised that this information will be
used as an invaluable baseline from which to demonstrate their progress with
training and practice. Since this is a pre-test to establish a baseline measure, it is
useful to record the subjects’ magnitude estimate of their threshold response on a 1–
10 scale. Such a measure is never, however, requested after any subsequent reinforcement training session. To do so would place emphasis on motion sickness—in
other words, on failure—whereas each subsequent exposure should aim at building
confidence. The counselor’s goal is for the subject to make progress by staying in
the motion environment for a longer time, feeling better, or both.
When the subject exits the training device, it is useful to give him or her a
helping hand. This is not merely because of any possible loss of balance, however.
It allows the counsellor to assess the presence of any palmar sweating as a measure
of motion sickness. It is also important to note, discreetly, the subject’s appearance,
with particular reference to skin pallor, signs of anxiety and unsteadiness. You will
note that these measures are all obtained without ever asking if the client feels sick
and don’t forget that motion sickness questionnaires are NEVER used. The counselor can then take these indicators into consideration when reviewing the overall
severity of the subject’s motion sickness response. There are good reasons for being
so careful during the first session. People who are prone to motion sickness often
have become used to persevering in a motion environment; this may cause them to
overestimate their ability to cope and, therefore, they may tend to go beyond their
true “threshold”, a feature that can slow them up.
12.5
12.5
Second Training Session
267
Second Training Session
Confirm the subject’s threshold of response.
Note the subject’s appearance and demeanor associated with that motion sickness response.
After the usual introductory remarks, it is useful to discuss with subjects how
they felt after their departure from the first training session. This is the only time
that this is done, so as not to dwell on negative responses during subsequent
training. Did any residual motion sickness symptoms diminish, and if so, how
quickly—or did they increase at all? The counsellor points out that some subjects
stay in the device somewhat beyond their threshold, because they have become
used to “hanging on” in such circumstances. These questions are aimed at assessing
whether or not the previous duration of exposure was a good indication of their
threshold or if the duration of exposure needs to be curtailed for this next session.
This is the only time that such questions are asked and they are couched in positive
terms are far as possible. Any questions or comments from the subject should be
addressed and examples of similar situations occurring to others should be offered.
Also it is valuable for subjects to be able to compare their own motion sickness
experiences with those of the general population, since this tends to lessen feelings
of isolation and uniqueness.
During desensitization training, in whatever device is used, be it in this rotating/
tilting chair or the Dichgans and Brandt optokinetic drum that we shall describe in
the next chapter and particularly in the early stages of either, it is useful to hold a
conversation with the subject, for two reasons. First, this helps to focus the subject’s
attention away from the training stimulus that we shall be using and reduce any
anticipatory fears. Second, it gives the counselor a good indication of the subject’s
motion responses to the training session and the situation generally. This is
important because we never ask if they are feeling motion sick—not ever! That
would undermine the subject’s confidence, which at this early stage of training is
particularly fragile. It is the counselor’s responsibility to make sure that the amount
of stimulation is within the ability of the subject to manage. It is useful once more to
give the subject a helping hand out of the device to check for the presence of
clamminess of the skin and compare the subject’s state with his or her condition
during the responses after the first session.
The main objective of this second exposure is to establish the subject’s response
threshold more positively, so the planned duration of this second session is based
upon all the information gained during the first session. This includes how the
subject felt during that session, the previous recorded duration of exposure and
magnitude estimate of motion sickness. Based on these data, the counselor plans the
duration of the next desensitization session, so as to ensure that he does not exceed
the subject’s threshold. As the planned duration of exposure approaches, the
counselor may decide to let the subject continue if all the cues seem positive. This is
where conversation is so useful. If the subject’s voice and flow of speech sound
normal and he or she seems involved in the conversation, one may allow extra time.
If, however, the subject becomes quiet or seems preoccupied, the session is stopped
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without comment. Bear in mind that you, the counselor have preplanned the
duration without informing the subject. As is the case in all subsequent sessions, the
duration and type of exposure are recorded; but in this case, unlike the first, there is
no request for estimates of sickness.
Even if the duration of this desensitization exposure happens to be less than
before, the counselor may still comment positively by saying that the session was
very good and useful in confirming the subject’s current threshold. If, on the other
hand, the duration was exceeded, one can also use that fact as positive encouragement for the subject.
12.6
Type Three Training Session
Introduce assessment of physical relaxation.
Continue to increase the duration of exposure within the subject’s threshold of response.
It is useful to begin this training session by discussing the subject’s state of
physical relaxation in a provocative environment by explaining a simple way to
evaluate this. It is important to stress physical rather than cognitive or mental
relaxation. The author believes that cognitive focus is most important and physical
relaxation is merely used as a measure of reduced arousal. The subject is advised to
“wiggle” the lower jaw from side to side quickly and to assess how loose or tight
the jaw muscles feel. The counselor demonstrates this action, showing the difference in the jaw movements between loose and tight jaw muscles. It is not necessary
for the subject to try to describe the sensation to the counselor; the information is
merely a base-line for future comparison by the subject. Having demonstrated this
and asked the subject to try it, they are told that they will be requested to do this
from time to time when they are in the motion environment and comment on any
change. It is useful to have them do this when they are seated in the chair, stationary; after set-up; midway during the planned exposure; just before the end of the
session, and after shut-down. Variations in jaw muscle tension give the counselor
an indication of how and when arousal is mounting and how well subjects are able
to relax physically. These responses should be explained positively as natural
reactions and that will be addressed in the next session.
The counselor plans the duration of desensitization on what has been achieved
during the previous session and the last assessment of the general state of the
subject when that session was over and he is getting out of the training equipment;
these features give him a pointer on how the subject had felt at the end of the
session. He also encourages the subject on his or her progress; as you will have
gathered, the idea is to gain all these various pointers on the state of the individual;
in other words, the counselor is being positive throughout.
12.7
12.7
Type Four Training Session
269
Type Four Training Session
Introduce the concept of points of attention as a protective maneuver.
Continue to increase stimulus duration within the subject’s ability to cope without motion
discomfort.
At the beginning of this session the counselor discusses focus of attention,
pointing out that if the individual concentrates hard on something totally unrelated
to the motion environment, dizziness and disorientation are lessened and it helps the
subject to relax physically.
Counselors have a choice in how they encourage a subject to focus his or her
attention. For example, casual conversation is not as powerful as structured tasks
along the lines that we have already described. To be really effective, the protective
tasks need to involve considerable mental concentration. The author has found that
counting backwards in threes (or some such number) or reciting the alphabet
backwards usually meets this requirement. If such a task is used, however, the
counselor should stress that this is merely a demonstration of the effectiveness of
focusing attention and in no way is it meant to suggest that this will be a permanent
feature of providing the subject’s protection in the future. A combination of this
technique (with assessments of physical relaxation) can then be demonstrated and,
it is hoped, that the protection offered by temporary periods of focusing attention as
suggested can then be established.
At this stage the counselor should plan 5–10% increments in the duration of
stimulation, but should always remain flexible and increase or decrease this time as
necessary to ensure that the subject is not made too uncomfortable; aborts should be
avoided at all cost.
12.8
Type Five Training Session
Continue practice with focus of attention, but becoming less structured; subject uses own
version.
Relate training responses to subject’s current progress in the real world.
The subject should now be making good progress in terms of increasing tolerance to the provocative stimulus, and also being more physically relaxed, and
leaving the device in a much more confident mood. The counselor makes every
effort to encourage this progress. The subject can now adopt his or her own way of
focusing attention, without recourse to earlier structured complex paradigms.
In addition, it is now useful to ask if any real-world experiences related to
motion have occurred recently. Subjects often repeat positive experiences in their
own world, such as terms of riding in automobiles or sailing, and these are
applauded by the counsellor as being useful indications that subjects are working
well on their own in terms of practicing this technique. The counselor must always
stress that the subject is the real leader in this training programme and the counselor
is merely the guide and sounding board.
270
12
Cognitive-Behavioural Desensitisation Training …
At this stage, tolerance to the motion stimuli should now be progressing well and
increments of 15% in terms of duration of each run are now being achieved. But
one must always remember that the actual amount of stimulation is still, as always,
a judgment to be made by the counselor during each session.
12.9
Type Six Training Session
Encouragement is particularly important around this stage of training for subjects who think
that their progress is “too easy” to be effective.
Over-confidence in other subjects should not be allowed to lead to premature termination of
training.
Experience has shown that around this time, average progress is very good;
subjects are much more relaxed and buoyant and no longer need to rely upon
artificial strategies to cope with provocative stimulation. Some subjects have a short
period of uncertainty, however; although progressing well they are somewhat
bewildered because they feel that they are not doing anything to help themselves
and so cannot understand why things are going well. The counselor should explain
that this is a natural reaction, because of their previous experiences and lack of
confidence with provocative motion. Counselors should stress that the subject is
making excellent progress and this is a typical reaction from a high achiever who
expects to have to make an effort to gain success. Point out that this feeling is
common and indicates that the subject really is progressing well and tackling
motion like those others whom they considered to be motion resistant. It is a good
sign that their anxiety overlay has markedly diminished or is gone altogether.
On the other hand, it is very important to guard against a subject’s
over-confidence at this stage. Some subjects become eager to end their training as
soon as they begin to feel better, but premature termination must be avoided
without destroying confidence. It is important not only to perform more than seven
sessions, but also to extend the training period over three or four weeks to allow the
subject to become accustomed to success.
Durations of exposure can now be pushed along with reasonable certainty that
the subject will respond positively; nevertheless one must keep a careful eye on
subject to make sure that he is not pushed too far at these times otherwise it might
send him or her back a bit.
12.10
Type Seven Training Session
Counselor begins to play a less active part in the training session in order to encourage
subject to stand alone.
This session is similar to the sixth, with planned increases in tolerance duration.
It is now worthwhile to begin to distance the counselor from the training session, as
12.10
Type Seven Training Session
271
a further step in boosting the subject’s confidence. This can be achieved by
reducing conversation with the subject, only occasionally making remarks unrelated
to the motion experience, thereby checking the subject’s response. A short conversation that takes place around the planned time for the end, or just before the end
of the time is a useful indicator of progress and allows training runs to be extended
with greater safety when the subject sounds positive; otherwise you may push the
subject too far and that can set him or her back a bit so it is also very important
before making that decision.
12.11
Type Eight Training Session
Continue to allow the subject to handle the stimulus environment with minimal support.
During the introductory remarks, the counselor can usually get a good indication
of the subject’s progress and level of confidence. Remarks such as “You must be
pleased with your progress, you ran for fifteen minutes last time, that is a significant
improvement,” usually cause the subject to expand on their feelings about their
ability to handle motion stimuli.
A good response allows the counselor to make some excuse to leave the area,
which also encourages the subject, because it indicates that the counsellor is now
confident in the subject’s increased ability to handle motion. This is a controlled
strategy in that the counselor continues to monitor the subject and training equipment discreetly from a suitable vantage point. At this stage, increases in tolerance
are usually planned for 15% or greater.
12.12
Type Nine and Subsequent Training Sessions
Increase duration and complexity of stimulation progressive as to enhance habituation
within subject’s now greatly increased ability.
End training programme at the subject’s request after at least 3 weeks of good progress.
By this stage the subjects commonly expresses confidence in their ability to
handle not only the stimulation in the test device, but real-world provocative motion
situations as well. They make great strides in terms of motion tolerance and leave
the device with smiles and expressions of confidence. Further sessions may or may
not be worthwhile, depending upon the individual. When subjects state that they are
doing well in the real motion world and are confident that they can now handle
situations which previously caused motion sickness, it is time to wind up the
programme because they have made the decision that motion sickness is no longer a
problem for them. No formal follow-up appointment is scheduled because this
might be considered as an indication of counsellor doubts and it is important that
subjects leave the programme on a high note.
272
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Cognitive-Behavioural Desensitisation Training …
Having achieved a successful outcome, subjects do not relapse. Unlike a
physical fitness or weight loss regimen, the failure rate does not seem to be a
consideration. Subjects feel that they can now tackle motion environments like
those individuals whom they thought to be naturally resistant. They also realize that
nobody is immune to motion sickness and that practice is important to increase the
level of habituation. What is different now is that in the future the subjects can enter
the provocative motion environment with minimal or no arousal and get their
“motion legs” just as do those without a history of severe motion sickness.
I must repeat that these original trainees have all failed their first pilot training
before they were sent to Dobie top take part in this Cognitive-Behavioural
Desensitisation trial as a means of being able to complete this training on their
second attempt. In order to satisfy the RAF Executive, their results were not
published until 5 years after the end of that training had been successfully been
completed as can be seen in the following Table 12.2, which confirms that 86%
successful pass rate from their new Cognitive-Behavioural Desensitisation training.
12.13
Summary
• Cognitive-behavioural training involves psychological, physiological, and
physical components that work together to reduce the heightened arousal that
sufferers of chronic motion sickness experience. The degree of arousal or
anxiety may vary with different types of provocative motion and different
individual expectations.
• Through the use of confidence building, habituation, and adaptation techniques,
cognitive-behavioural training has been beneficial to those in the RAF who have
been grounded due to this malady of motion sickness. It has also been used
successfully to overcome seasickness, carsickness and other forms of motion
sickness in both military and civilian clients.
References
Barlow LN (ed) (1946) Charles Darwin and the Voyage of the Beagle. Philosophical Library, New
York, NY
DePuy WH (1896) Sea-sickness. In: The Encyclopædia Britannica, a dictionary of arts, sciences,
and general literature, vol XXI. The Werner Company, MDCCCXCVI, Chicago
Dobie TG (1965) Motion sickness during flying training. In: AGARD conference proceedings
No. 2, North Atlantic Treaty Organization Advisory Group for Aerospace Research and
Development, Neuilly-sur-Seine, France, p. 23
Dobie TG (1971) The disorientation accident—philosophy of instrument flying training. In: The
disorientation incident. AGARD conference proceedings, AGARD-CPP-95-71, North Atlantic
References
273
Treaty Organization Advisory Group for Aerospace Research and Development,
Neuilly-sur-Seine, France, vol A15, pp. 1–3
Dobie TG (1974) Airsickness in aircrew. AGARDOGRAPH No. 177, North Atlantic Treaty
Organization Advisory Group for Aerospace Research and Development, Neuilly-sur-Seine,
France
Dobie TG, May JG, Fisher WD, Bologna NB (1989) An evaluation of cognitive-behavioral
therapy for training resistance to visually-induced motion sickness. Aviat Space Environ Med
60:307–314
Golding JF, Stott JRR (1995) Effect of sickness severity on habituation to repeated motion
challenges in aircrew referred for airsickness treatment. Aviat Space Environ Med 66:625–630
Wendt GR (1948) Of what importance are psychological factors in motion sickness? J Aviat Med
19:24–33
Chapter 13
Experimental Evaluation
of the Components
of Cognitive-Behavioural Training
Using Illusory Motion in
an Optokinetic Drum
Abstract When I first proposed my course of cognitive-behavioural desensitisation
training, it generated its fair share of adverse comments. For a start, the naysayers
believed that I was only putting off the evil day and all of my clients would fall by
the wayside sooner or later with a resumption of motion sickness. The programme
would simply waste time and money. Others believed that it was merely a behavioural desensitising programme and there was no point in the so-called cognitive
component. I would very much like to have addressed the latter issue at that time,
but was convinced that both were necessary and above all, my clients only had one
shot for success. As to the former question, only time would tell. Finally, there was
no question of having a control group for ethical reasons. I am pleased to tell you
that I have been able to address these issues since then and the answers are to be
found in this chapter.
When I left the Royal Air Force, a number of important questions concerning
cognitive-behavioural training remained to be answered. Was there a need for the
cognitive component in the programme or was the effectiveness of the technique
entirely due to repetitive behavioural desensitisation? If the cognitive component
was important, how easy would it be to train counsellors, and furthermore, to be
successful did a counsellor need to have both a medical and flying background like
myself, to be convincing? Did cross-coupled (Coriolis) stimulation provide an
adequate and appropriate desensitisation stimulus for managing airsickness? If so,
would that same type of desensitisation stimulus translate to the acceleration profiles that caused seasickness or any other form of motion sickness? How effective
was cognitive-behavioural training compared with other therapeutic methods, such
as biofeedback? When using my cognitive-behavioural training programme in the
RAF, all of my clients were flight crewmembers who were being permanently
grounded due to apparently chronic intractable airsickness. These individuals had
only 4 weeks left in which to be recovered as flight crew personnel. I did not
consider that it would be ethical, or practical, to treat some of these persons as a
control group in order to evaluate the effectiveness of the constituent parts of the
programme, since they only had that one chance for success.
© Springer Nature Switzerland AG 2019
T. G. Dobie, Motion Sickness, Springer Series on Naval Architecture,
Marine Engineering, Shipbuilding and Shipping 6,
https://doi.org/10.1007/978-3-319-97493-4_13
275
276
13
Experimental Evaluation of the Components …
It was not until I returned to the study of motion sickness at the Naval
Biodynamics Laboratory (NBDL), now known as the National Biodynamics
Laboratory, part of the University of New Orleans, and collaborated with Dr. James
May in the Department of Psychology at the same University, that we had the
opportunity to investigate these matters further. We carried out a number of studies
to examine these interesting questions and, at the same time, took the opportunity to
evaluate the effectiveness of this method of training to manage forms of motion
sickness other than simply the original problem of airsickness; that I was faced with
in the Royal Air Force. These studies are summarised here.
13.1
Equipment Used for Visually-Induced Apparent
(Illusory) Motion
Originally I had used cross-coupled (Coriolis) passive vestibular stimulation when I
first developed cognitive-behavioural anti-motion sickness training. When I first
arrived at the Naval Biodynamics Laboratory, there had been no suitable equipment
available to provide provocative motion stimulation. However, in the Department
of Psychology at the University of New Orleans (UNO), I was able use a Dichgans
and Brandt (1973) type of optokinetic drum. It produced visually-induced illusory
motion as an alternative to cross-coupled (Coriolis) stimulation. This provided me
with the opportunity to investigate the effectiveness of illusory motion as a
desensitising stimulus, in a cognitive-behavioural setting, for managing motion
sickness, bearing in mind that I was interested in providing a motion response and
not a specific type of stimulus. For that reason, the optokinetic drum should also be
quite satisfactory (Fig. 13.1).
13.2
UNO Optokinetic Drum
The UNO optokinetic rotating drum (Fig. 13.2) had been constructed to provide
whole-field visual stimulation. It consisted of a large cylinder, 5 ft. (1.5 m) in
diameter and 4 ft. (1.2 m) high, fabricated from lightweight tubing and lined with a
continuous white plastic inner shell. There were 5 in. (15 cm) alternating
black-and-white stripes on the inner surface of the drum. The ceiling of the drum
was mirrored so that the stripes were effectively “extended” upwards to fill the
entire visual field (Fig. 13.3). The drum was attached by a suspension platform,
which, in turn, was connected to ceiling anchors by cables. This system allowed the
apparatus to be leveled and prevented the suspension platform from oscillating
during drum rotation. The rotational speed of the drum, which was driven by a
direct current motor, could be controlled from less than 1 rpm to more than 18 rpm.
13.2
UNO Optokinetic Drum
277
Fig. 13.1 Dichgans-and-Brandt type of optokinetic drum (outside view) as used at the University
of New Orleans
A small, sturdy, raised platform had been built to hold a fixed chair on which the
subject sat during training. When seated, the subject’s head was positioned close to
the drum’s rotational axis, just above midway between the upper and lower margins
278
13
Experimental Evaluation of the Components …
Fig. 13.2 Dichgans-and-Brandt type of optokinetic drum (inside view), showing subject’s seat
and mirror in ceiling as used at the University of New Orleans
of the cylinder. However, the subject was required to look at the inner wall of the
drum some 4 in below the mirrored ceiling; this ensured that the rotating stripes or
their reflections filled the whole visual field. A headrest was provided for stability.
A stop button on the arm of the chair, convenient to the hand, allowed a subject to
terminate the exposure to provocative motion if a point of intolerance, or motion
sickness threshold, as the case might be, was reached.
13.3
Circular Vection
Shortly after the drum started to rotate, the subject, who was physically stationary at
all times on the fixed seat, experienced the illusion that the drum was slowing down
or stopping and that he or she was rotating bodily in the direction opposite to that in
which the drum has been rotating. This experience, known as circular vection, is a
peripheral visual phenomenon. Vection caused the majority of subjects to experience disorientation that led to the onset of motion sickness. Extensive investigation,
including more than 100 subjects, has shown that 40% of those tested described
moderate to severe motion sickness. Stern et al. (1989) have reported that in their
13.3
Circular Vection
279
Fig. 13.3 National Biodynamics Laboratory rotating/tilting chair equipped with a projection
module
experience, circular vection provoked motion sickness in approximately 60% of
healthy subjects.
In this context, Hu et al. (1991) have addressed the question: “Does self-motion
cause the development of visually-induced motion sickness?” They believed that
this illusory perception of self-motion played an important role in causing motion
sickness. They carried out a multivariate correlation that showed that vection had a
significant effect on the severity of motion sickness. They also observed, however,
that the illusion of vection varied among individuals. They found that most people
who reported strong vection in an optokinetic drum developed severe symptoms of
motion sickness, whereas others who failed to experience saturated vection also
became very sick. This has also been the experience in our laboratory.
280
13
Experimental Evaluation of the Components …
Yang and Pei (1991) studied the effects of different combinations of vection and
head movements on the severity of motion sickness. In this case, they tested a
population of 26 subjects in a hollow fiberglass rotating sphere lined with randomly
spaced black dots of different sizes, on a white background. The sphere could be
rotated about a vertical or horizontal axis at a speed of 45°/s. This resulted in
vertical yaw, horizontal roll, or pitch vection. Coincidentally with the rotation of the
sphere, the subjects actively moved the head through 20° in the pitch, roll, or yaw
planes, at a frequency of 0.5 Hz. Yang and Pei found that vection in the yaw plane,
combined with pitch or roll movements of the subject’s head, increased the severity
of the resulting motion sickness significantly. On the other hand, pitch vection
combined with any kind of head movement or rotation of the head and scene about
the same axis, have both significantly reduced the motion sickness response. They
further reported that if the head was kept stationary, pitch vection produced the
greatest motion sickness response, followed by roll vection, then yaw vection. Yaw
vection has given the strongest illusion of self-rotation, followed by roll vection
and, least of all, pitch vection. As Yang and Pei pointed out, their results were the
same as those for head movements in terms of provoking motion sickness.
In a different study, Hu et al. (1996) investigated the relationship between a
person’s history of motion sickness and their susceptibility to motion sickness in a
rotating optokinetic drum. Forty-nine subjects participated in this study, of whom
25 were female and the other 24 male. The subjects’ ages ranged from 18 to
25 years. Each subject was seated in the stationary drum for a 12-min period as a
baseline and was then exposed to visually-induced apparent motion in the rotating
drum for a further period of 12 min. Subjects were required to sit still and look
straight ahead at the rotating stripes; their drum was longer than ours so they were
able to do that without seeing outside the bottom of the drum. We overcame that
shortcoming by extending the illusory stripes with the mirror. Electrogastrograms
were recorded during the period of rotation and a motion sickness questionnaire
related to symptomatology during rotation was completed at the end of each
exposure to circular vection. The motion sickness history questionnaire was scored
by a method described by Reason and Brand (1975).
Hu et al. found significant correlations between the subjects’ motion sickness
history scores and those obtained during illusory motion in the optokinetic drum.
They also noted a positive relationship between the motion sickness history scores
and the electrogastrogram 4–9 cycles/min (cpm) spectral intensity ratios recorded
during drum rotation and the baseline periods. Hu et al. reported that the mean
motion sickness symptomatology scores during the period of exposure to drum
rotation were 11.50 for those subjects whose motion sickness history scores had
been in the top 33%; 4.18 for the middle 34% scorers; and 1.21 for the bottom 33%.
In addition, the mean 4-9 cpm spectral intensity ratios of the electrogastrograms
between illusory motion and baseline periods have been 2.62 for those in the top
33% of motion sickness history responders; 1.44 for the middle 34%; and 1.21 for
the bottom 33%. Hu et al. concluded that their results have shown that a subject’s
13.3
Circular Vection
281
history of motion sickness has correlated well with the severity of motion sickness
experienced during illusory motion in an optokinetic drum.
Stern et al. (1989) carried out an investigation to assess motion sickness and
electrogastrographic (EGG) responses to 3 repeated exposures to circular vection in
an optokinetic drum, at a rotational speed of 60°/s, during which the subjects’
gastric myoelectrical activity was recorded and they reported their motion sickness
responses. In their first experiment with 10 subjects, the intersession intervals
between the 3 exposures to illusory motion have been 4–24 days. The subjective
motion sickness reports from these subjects, all of whom have shown tachygastria
as indicated by an abnormal 4–9 cpm gastric rhythm, failed to indicate adaptation.
In a second experiment with 14 new subjects in which the intersession intervals
were reduced to 48 h, however, the group experienced a reduction in both their
symptoms of motion sickness and associated tachygastria. This seemed to support
the notion that adaptation to motion sickness induced by vection could occur after 3
exposures, if the intersession intervals were around 48 h, whereas 4–24 days was
too long; this supported the findings of Reason and Brand (1975).
Stern et al. (1990) also investigated the effects of visual fixation and a restricted
field of view on motion sickness induced by circular vection in an optokinetic drum.
They stated that while the drum was rotating it had been generally assumed that a
mismatch has occurred because the subject has experienced illusory self-motion
while the vestibular and proprioceptive sensory inputs were indicating that the body
was stationary. They pointed out, however, that there has been another potential
conflict due to incompatible eye movements. In this study, they compared circular
vection with nystagmus during illusory motion, with and without restricted visual
fields, while recording the severity of motion sickness. Subjects were randomly
assigned to one of three groups: first, a control group with an unrestricted view of
the inner surface of the drum; second, a group of subjects whose field of view was
restricted to a 15° circle; third, a group that fixated on a 1 cm black cross. The cross
was located 25 cm before their eyes and 10 cm from the inner surface of the drum.
The results have shown that nystagmus has been markedly suppressed in the
group fixating on a target and partially reduced in the group with a restricted field of
view, in comparison with the unrestricted control group. In terms of vection, the
fixation group reported a significant reduction compared with the control group. As
one would expect, the restricted field group reported the least amount of vection. In
the control group, the symptoms of motion sickness increased throughout the
12 min of exposure to illusory motion, whereas there were only a few reports of
symptoms in either the fixation or restricted field groups. In these 2 groups, there
were no reports of nausea, whereas 8 of the 15 subjects in the control group
experienced nausea. In similar fashion, tachyarrhythmia, as recorded by an electrogastrogram, was significantly greater in the control subjects than those in the
other 2 groups, but not during the baseline or recovery periods. These workers have
stated that since the fixation group has experienced more vection and less
282
13
Experimental Evaluation of the Components …
nystagmus than the restricted field group, this has indicated a partial dissociation of
vection and nystagmus. To some extent, this has dissociated the conflict produced
by eye movement and illusory self-motion. They were, however, unable to make a
quantitative comparison of the relative significance of the incompatibility of eye
movements and self-motion.
In our laboratory at UNO, we conducted a study similar to that of Stern et al.
(Flanagan et al. 2002), except that we used a wider field of view, in the restricted
field of view conditions, thereby attempting to restrict illusory vection without
limiting optokinetic nystagmus. We also measured the duration and amplitude of
nystagmus as well as subjective measures of vection. The results revealed that
visual fixation reduced vection to levels similar to those produced by a restricted
field of view. The mean estimate of vection in the fixation condition was slightly
lower than with a restricted field of view. Our restricted field of view did not
preclude nystagmus, however the mean amplitude was shown to be significantly
less than for a full field of view. Our results have indicated that a reduction in eye
movements caused a reduction in the magnitude of the perception of vection that
might contribute to a reduction in motion sickness. Both eye movements and
sensory conflict might well be involved in the aetiology of motion sickness
resulting from illusory motion.
13.4
NBDL Desensitisation Chair
I had also arranged to have a rotating/tilting chair built at the National Biodynamics
Laboratory (NBDL) to provide passive cross-coupled (Coriolis) stimulation, based
on the design of my original RAF equipment (Fig. 12.3). The specifications of both
chairs were similar. The NBDL chair (Fig. 13.4) incorporated a viewing screen and
a slotted cylinder above the subject’s head that provided rotating vertical linear
shadows on the screen. These simulated the rotating black and white stripes on the
inside of the Dichgans and Brandt type of optokinetic drum used at UNO. This type
of simulation had drawbacks, however, since any flaws on the screen were stationary and tended to cancel the illusion of vection. In the optokinetic drum, a flaw
on the interior surface had no such detrimental effect because it formed part of the
rotating (illusory) stimulus; as the stripes rotated so did the “flaw.” This problem
has been overcome in other laboratories by projecting small white symbols onto a
black surface.
A second rotating/tilting chair was then built and mounted inside a mobile trailer
to transport the device to other locations to carry out field studies or cognitivebehavioural programmes for personnel at these locations (Fig. 13.5).
13.4
NBDL Desensitisation Chair
283
Fig. 13.4 Motion desensitisation chair housed in the National Biodynamics Laboratory Mobile
Biodynamics Laboratory (insert)
Fig. 13.5 Mean tolerance scores for each group obtained during two pre-tests and post-test
284
13.5
13
Experimental Evaluation of the Components …
Evaluation of Key Components
of Cognitive-Behavioural Desensitisation Training
When I first published the concept of cognitive-behavioural training in 1974, as a
way of managing chronic motion sickness, queries had been raised concerning the
need for the cognitive component. It had been suggested that the protective effects
of this programme have perhaps been due entirely to the behavioural desensitisation
element and the so-called cognitive portion was unnecessary. Clearly, this was a
very important issue that required an answer.
In a UNO experiment (Dobie et al. 1989), we have evaluated the relative
advantages of the cognitive (counselling) component, as compared to behavioural
desensitisation alone, for training resistance to visually-induced apparent motion in
an optokinetic drum. The 32 subjects (22 female and 10 male) ranged in age from
16 to 69 years. Only subjects who had: a positive history of motion sickness as
indicated by questionnaire; extremely low tolerance scores on a pre-test involving
visually-induced motion sickness; and a negative history of labyrinthine disorders,
were selected for this programme.
The 32 test subjects were assigned to one of four groups matched in relation to
their average motion sickness susceptibility and tolerance to illusory motion. After
being assigned to their groups, the subjects were then given a second pre-test to
establish the test-retest reliability in terms of their tolerance measures. Immediately
before and after this pre-test, subjects used a checklist to report any of the common
symptoms of motion sickness. They were also asked to give magnitude estimates
(on a scale of 0–10) of self-vection drum movement, and severity of motion
sickness immediately after terminating the test.
The “cognitive counselling only” group of subjects received ten sessions of
confidence building counselling. The “desensitisation only” group received ten
sessions of exposure to illusory motion in the optokinetic drum, with neither
supportive counselling nor encouragement from the experimenter. The duration of
exposure to illusory motion during the first session has represented 75% of the
subject’s initial pre-test endurance. In Sessions 2 and 3, an attempt was made to
increase the duration with increments of 5% and the remaining sessions by increments of 15%. These values have been derived from the actual increases in duration
of exposure that were obtained in another experiment. The “cognitive-behavioural
training” group received both the confidence-building counselling and repeated
exposure to the illusory visual stimulus. The first session was identical to that of the
“cognitive-only” group, but sessions 2 through 10 were 20 min each in length,
combining confidence building with desensitisation training. The experimenter
planned the duration of exposure of subjects, during desensitisation training,
according to the client’s progress. The aim has been to achieve approximately 75%
of the pre-test latency for the first session followed by increments of 5% for sessions 2 and 3 and the remaining sessions by approximately 15%. The subjects in the
“control” group received ten 30-min sessions of subject/(non-involved) experimenter interaction on matters entirely unrelated to motion sickness. Like all the
13.5
Evaluation of Key Components of Cognitive-Behavioural …
285
other subjects in the study, they have undergone a post-test in the drum 30 days
after screening.
The results have shown that only the two groups that received cognitive counselling demonstrated significant increases in tolerance to visually-induced apparent
motion (Fig. 13.6) together with decreases in their associated symptoms of motion
sickness (Fig. 13.7). In addition, the group that received both cognitive counselling
and desensitisation training showed significantly increased tolerance to
visually-induced apparent motion when compared to the group that received cognitive counselling alone. During desensitisation training, the duration of exposure to
visually-induced apparent motion was determined by the subjects themselves, since
they had been instructed to abort the procedure if they reached a point of undue
motion discomfort. None of the subjects in the group that received the combined
(cognitive-behavioural) treatment had aborted during any of the desensitisation
sessions. On the other hand, every subject in the “desensitisation only” group
aborted the exposure during at least two such sessions (Table 13.1).
It is likely that this response reflected the heightened arousal experienced by
these subjects. This matter of arousal had been dealt with in those groups that
received counselling and the subject’s increased confidence tended to prevent
aborts. These results have indicated that mere repetitive exposure to provocative
stimulation by means of visually-induced apparent motion stimulation had not been
sufficient to reduce motion sickness.
The main finding in this experiment has been that cognitive-behavioural training
provided significant support for those individuals who have been highly susceptible
to visually-induced motion sickness. The results have also suggested that neither
the cognitive nor the desensitisation component alone has been responsible for the
significant increase in resistance to visually-induced disorientation, but that the
combination is most effective. It is important to note, however, that since the
Fig. 13.6 Mean
symptomatology scores for
each group obtained
immediately after termination
of visually-induced apparent
motion stimulation during two
pre-tests and the post-test
286
13
Experimental Evaluation of the Components …
Fig. 13.7 Mean tolerance scores for each group obtained during two pre-tests and the post-test
Table 13.1 Aborted sessions during desensitization training
Subjects
a
b
c
d
e
f
g
h
Total aborts
by session
Sessions
1
2
3
4
5
6
■
■
■
■
■
1
■
■
■
7
3
■
4
9
■
3
■
■
■
■
5
10
■
■
■
■
■
3
8
■
■
■
■
■
■
3
■
4
Total aborts
by subject
3
3
4
3
2
2
4
5
cognitive-only group exhibited significant improvement over control, this fact
strongly supports the argument for a counselling approach to the treatment of
motion sickness. It is also apparent that frequent experience with the provocative
disorienting stimulus is needed to reap the full benefit of such counselling, in most
subjects, presumably by reinforcing their newly found confidence by example.
These positive experiences with provocative motion support the idea that subjects
who have apparently been sensitive to motion can in practice handle these stimuli
successfully, as do those others who are apparently “resistant” to motion. Since the
desensitisation-only group has not differed from the control group, it has been made
clear that purely behavioural training alone is unlikely to provide a satisfactory
13.5
Evaluation of Key Components of Cognitive-Behavioural …
287
management technique. Perhaps this is a reflection of the fact that the majority of
chronic sufferers of “car sickness” do not improve despite riding regularly in an
automobile. It was also apparent from the performance of the “cognitive-only”
group of subjects (who had no behavioural desensitisation training at all) that actual
exposure to provocative motion has not been essential to acquire significant tolerance to such stimulation. These findings have emphasised the importance of
cognitive factors in both understanding and managing motion sickness.
13.6
Counsellor Training
All of the previous experiments, both here and in the UK, have involved the same
counsellor, namely myself, so we had been faced with the question as to whether
these training procedures would be effective in the hands of other individuals. In
order to address this issue, we developed a course of instruction to teach counselling to a population of college students and Navy personnel. These consisted of 4
psychology graduate students, 6 psychology undergraduate students, 3 business
undergraduate students, 1 naval officer, and 2 Navy enlisted men. Two business
majors dropped out of the course after the first session and a psychology major
dropped out after five sessions. However, these particular individuals indicated that
personal time constraints alone had prohibited further participation in the programme. The course was planned to consist of 12 2-h, biweekly sessions, followed
by a final examination.
Benson’s (1988) review chapter, entitled “Motion Sickness,” was assigned as
essential reading for the course. The syllabus covered the following topics: background information, visually-induced apparent (illusory) motion, models of motion
sickness, psychological theory, learning and motion sickness, counter-conditioning
and desensitisation, cognitive-behavioural counselling, expectations and positive
thinking, confidence building, desensitisation training, experimental evidence, and
has included a demonstration of a simulated counselling session.
We administered a 50-item multiple-choice examination during the last session
and the responses were then machine scored. Grades ranged from 66 to 96%
correct, with a mean of 85.5% and a standard deviation of 7.7%. The examination
was also administered to a group of college students who had not received the
course of instruction. The results have shown that these untrained individuals
scored far worse than the class, with only one individual having scored higher than
the worst score obtained by a member of the class. A one-way analysis of variance
has revealed a significant difference between the mean scores for the two groups.
We concluded that the test had been appropriate and that the class performed quite
well.
288
13
Experimental Evaluation of the Components …
However, that was only part of the answer. The critical question had remained.
How successfully would these candidates use cognitive-behavioural training to help
clients suffering from motion sickness to overcome their problem? In order to
answer that question, we then carried out an assessment of the outcome of their
counsellor training by means of a realistic field test. Eleven of the 13 volunteers
who had completed the course of instruction in cognitive-behavioural counselling
were recruited to act as counsellors in this second phase of the study. Four of the
potential counsellors were undergraduate psychology majors (1 male and 3 female);
4 were graduate students in psychology (1 male and 3 female); one naval officer (a
male with a B.A. in psychology); and two Navy enlisted men. Nine of the 11
counsellors were assigned 2 clients each and the 2 remaining counsellors were each
assigned 1 client. We then instructed all of the counsellors to employ the form of
cognitive-behavioural training that they had been taught in the previous phase of
this programme.
The test scores of clients counselled by those trainees were then compared with
those of clients counselled by myself, the experienced counsellor. The results
indicated that the trainees’ clients exhibited significant post-test increases in tolerance to visually-induced apparent motion, although not as great as those by the
experienced counsellor. Similar significant decreases in symptoms of motion
sickness were also noted. (Dobie and May 1995).
13.7
Optimal Number of Training Sessions
During my early work with RAF flight crews, the number of training sessions
(N > 20) employed in the cognitive-behavioural training programme had been
extensive because of the ample time available for training. In our more recent work,
however, the number of sessions has been somewhat arbitrarily fixed at ten. In this
study, we addressed the question of the optimal number of sessions that might be
employed in this type of management (Dobie and May 1996). Preliminary results
indicated that subjects receiving more sessions tend to achieve greater tolerance, but
there seemed to be a diminishing rate of return after about seven sessions. It is
probably good practice to tailor the number of sessions to the individual client’s
progress with a view to using at least seven to ten sessions over a period of three to
four weeks for the most beneficial results.
In conclusion, there are two factors at play here. First, is the total number of
training sessions, but in my view it is equally important to address a second issue,
namely the period of time over which these sessions take place. I strongly believe
that it is particularly important to perform this training over at least a three-week
period, in order to allow the benefits to “sink in.” The positive adjustment to a
subject’s feeling of confidence takes time to occur, particularly if the history of
motion sickness has been of long standing.
13.8
13.8
Comparison with a Biofeedback Technique
289
Comparison with a Biofeedback Technique
As pointed out in Chap. 11, Levy et al. (1981) described a US Air Force programme in which aircrews were provided with relaxation training in a two axes
chair, involving biofeedback. Cowings and Malmstrom (1984) also suggested that
training in biofeedback techniques is a useful means of teaching subjects how to
control the disruptive discomfort of provocative motion. Early experiments showed
that animal (Miller 1969) and human subjects (Elder et al. 1981; Kimmel 1974) can
learn to control these “involuntary” biological responses. Since autonomic measures known to be associated with provocative motion can be identified, this
method might be thought to offer advantages for teaching individuals how to
counteract these motion-induced discomforts. Both the Canadian Forces and the
United States Navy employed biofeedback in their anti-motion sickness training
programmes (Banks et al. 1992; Bower et al. 1993). At UNO we had experienced
psychologists in clinical biofeedback therapy, so we compared cognitivebehavioural training and a recognised clinical form of biofeedback aimed at promoting relaxation (Dobie et al. 1987).
In this study, we selected 16 subjects from a pool of 704 college students who
had completed a motion sickness history questionnaire (MSQ) and had been given a
pre-test by means of illusory motion in our optokinetic drum. Based upon their
MSQ responses, subjects were categorised according to various levels of their
reported history of motion sickness, as described in Table 13.2. In this study, 14 of
the subjects were taken from category G4, which indicated that they had experienced many of the signs and symptoms of motion sickness in a number of motion
environments. One subject was taken from both category G2 and G1 because our
initial screening test had shown that these two individuals were highly susceptible
to motion sickness caused by illusory stimulation, despite their somewhat negative
history for motion sickness
Table 13.2 Groupings of subjects by motion sickness history
Group
designation
Number
Criteria
G1
150
G2
399
G3
114
G4
41
No history of motion sickness despite wide experience with
motion sickness-provoking stimuli
Mild (few) symptoms of motion sickness on the motion stimuli
experienced
Suffered a number of signs and symptoms of motion sickness
during some of the motion stimuli experienced, including some at
greater than mild severity
Suffered significantly from motion sickness, experiencing a wide
variety of signs and symptoms in all the motion environments
experienced; severe responses being in the majority
Total
704
290
13
Experimental Evaluation of the Components …
All subjects were given a standard briefing concerning the effects of exposure to
illusory stimulation in an optokinetic drum and instructed to terminate the run by
pressing the stop button provided, if their motion sickness responses became
uncomfortable. All subjects were then given two pre-tests (involving response to
illusory stimulation before treatment began) and one post-test after the training
protocols had been completed. The duration of exposure for each subject was
recorded for each of the three tests. The same person, who had not been involved in
the counselling, supervised all illusory stimulation tests. Subjects were subjected to
drum stimulation at a constant rate of 10 rpm (i.e., 60°/s velocity of the inner
circumference of the cylinder). Both prior to entry into the drum and immediately
after termination of the illusory stimulation, all subjects completed a motion sickness symptomatology questionnaire. Based on the tolerance scores to illusory
motion obtained during the two pre-tests, to evaluate test/retest reliability, the 16
subjects were randomly assigned to one of four treatment groups.
The first group received clinical biofeedback training from an experienced
practitioner. Electromyogram (EMG) biofeedback, using forehead placement of the
electrodes, was selected as one of the modalities by which subjects in this group
were trained to relax. Because arousal of the sympathetic nervous system has not
always been correlated with levels of muscle tension, hand temperature biofeedback
was also employed. The value of thermal biofeedback in teaching patients to relax
has been demonstrated many times (Lashley and Elder 1984, 1982). In addition, the
advantages of simultaneous EMG and thermal (multimodal) biofeedback were
demonstrated by the same investigators whose clinical case data have suggested the
synergistic effects of multimodal biofeedback. It was also demonstrated experimentally when Gamble and Elder (1983) factorially compared thermal biofeedback,
EMG biofeedback and progressive muscular relaxation. For these reasons we
selected EMG and temperature feedback as the basis for our relaxation training
procedures.
The second group received cognitive-behavioural training from Dobie. Subjects
were given ten sessions of standard combined cognitive-behavioural training in
which an individual was given confidence-building counselling together with
desensitisation training, using, in this study, visually-induced apparent motion
stimulation.
The third group received concurrent sessions of both biofeedback and
cognitive-behavioural training, in every way identical to the procedures that have
been described for these forms of management, and the same counsellors were
used. Both therapists were unaware that the subjects in this group had also been
receiving another form of training.
A control group of subjects has participated in an experiment concerned with the
duration of spiral after-effects and magnitude estimation of the heaviness of
weights. There were five two-hour sessions. The experimenter who was supervising
this control group made no reference to the motion sickness project at any time.
When the pre- and post-training measures were compared, it was found that the two
groups receiving cognitive-behavioural training exhibited a significant increase in
their ability to tolerate visually-induced apparent motion (Fig. 13.8).
13.8
Comparison with a Biofeedback Technique
291
Fig. 13.8 Mean symptomatology scores for each group obtained immediately after termination of
visually-induced apparent motion stimulation during two pre-tests and the post-test
In addition, these two groups also reported a decrease in the symptoms associated with motion sickness (Fig. 13.8). Although the subjects in the biofeedback
group were successful in learning to control EMG activity through biofeedback,
these gains were not identified with the provocative motion environment and had
apparently provided the subjects little protection when they were post-tested.
Neither the group receiving biofeedback therapy alone nor the control group
demonstrated significant differences in pre- and post-test measures.
We concluded from these results that relaxation per se is not sufficient to explain
the success of cognitive-behavioural training. On the contrary, I would suggest that
relaxation involves both mental as well as physical relaxation, whereas in
cognitive-behavioural training, the subject is trained to remain mentally focused
and a relaxed physical state is only used to indicate a reduction in arousal.
The findings of this study support the efficacy of cognitive-behavioural training
for increasing tolerance to provocative stimulation that causes motion sickness. In
the first experiment in this series, dealing with the key components of
cognitive-behavioural training, the desensitisation-only group had not differed from
the control group. This finding called into question any suggestion that this aspect
of the combined treatment, in the present study, has been responsible for the differences between biofeedback and the cognitive-behavioural approach. These
results strongly suggest that a training protocol that includes a combination of both
confidence-building counselling and behavioural desensitisation deserves serious
consideration as a means of preventing motion sickness. This is in keeping with the
results already obtained with the same technique in a different setting where
cross-coupled (Coriolis) vestibular stimulation has been used in a
cognitive-behavioural training programme to desensitise flight trainees apparently
suffering from chronic incapacitating airsickness (Dobie 1974). These results have
292
13
Experimental Evaluation of the Components …
also tended to support my notion that the particular type of provocative stimulus
used in training does not have to simulate the motion that has been causing the
problem. On the contrary, there seem to be advantages in using an unfamiliar
stimulus. I stress again that this training programme is based on managing the
response and not the stimulus.
13.9
Theoretical Considerations
These experiments have answered most of the outstanding queries that were raised
concerning my cognitive-behavioural approach to the management of motion
sickness. In particular, they have confirmed the importance of the cognitive component in the cognitive-behavioural anti-motion sickness desensitisation training
programme and the fact that it is a practical and valid method to employ.
13.10
Summary
• Key components in motion sickness adaptation training include both a counselling element and a motion desensitisation component.
• A training protocol that includes a combination of confidence building counselling and behavioural desensitisation training deserves serious consideration as
a means of preventing motion sickness.
References
Banks RD, Salisbury DA, Ceresia PJ (1992) The Canadian Forces airsickness rehabilitation
program. Aviat Space Environ Med 63:1098–1101
Benson AJ (1988) Motion sickness. In: Ernsting J, King P (eds) Aviation medicine, 2nd edn.
Butterworth-Heinemann Ltd., Oxford
Bower EA, Clark JB, McCoy JG, Rupert AH (1993) Recent Navy experience in self paced
airsickness. Aviat Space Environ Med. In: 64th. Annual Scientific Meeting Program Abstract
#15
Cowings PS, Malmstrom FV (1984) What you thought you knew about motion sickness isn’t
necessarily so. Flying Saf 53:570–575
Dichgans J, Brandt T (1973) Optokinetic motion sickness as pseudo-Coriolis effects induced by
moving visual stimuli. Acta Otolaryngol 76:339–348
Dobie TG (1974) Airsickness in aircrew. AGARDOGRAPH No. 177, North Atlantic Treaty
Organization Advisory Group for Aerospace Research and Development, Neuilly-sur-Seine,
France
Dobie TG, May JG (1995) The effectiveness of a motion sickness counseling program. Br J Clin
Psychol 34:301–311
References
293
Dobie TG, May JG (1996) The optimal number of counseling sessions for the prevention of
motion sickness. NBDL-96R001, Naval Biodynamics Laboratory, New Orleans, LA
Dobie TG, May JG, Fisher WD, Elder ST, Kubitz KA (1987) A comparison of two methods of
training resistance to visually-induced motion sickness. Aviat Space Environ Med 58(9,
Suppl.):A34–41
Dobie TG, May JG, Fisher WD, Bologna NB (1989) An evaluation of cognitive-behavioral
therapy for training resistance to visually-induced motion sickness. Aviat Space Environ Med
60:307–314
Elder ST, Geoffray DJ, McAfee RD (1981) Essential hypertension: a behavioral perspective. In:
Haynes SM, Gannon L (eds) Psychosomatic disorders: a psychophysiological approach to
etiology and treatment. Praeger Press, New York, NY
Flanagan MB, May JG, Dobie TG (2002) Optokinetic nystagmus, vection and motion sickness.
Aviat Space Environ Med 73:1067–1073
Gamble EH, Elder ST (1983) Multimodal biofeedback in the treatment of migraine. Biofeedback
Self Regul 8:383–392
Hu S, Grant WF, Stern RM, Koch KL (1991) Motion sickness severity and physiological
correlates during repeated exposures to a rotating optokinetic drum. Aviat Space Environ Med
62:308–314
Hu S, Glaser KM, Hoffman TS, Stanton TM, Gruber MB (1996) Motion sickness susceptibility to
optokinetic rotation correlates to past history of motion sickness. Aviat Space Environ Med
667:320–324
Kimmel HD (1974) Instrumental conditioning of autonomically mediated responses in human
beings. Am Psychol 29:325–335
Lashley J, Elder ST (1982) Selected case studies in clinical biofeedback. J Clin Psychol 38:531–
540
Lashley JK, Elder ST (1984) Some biofeedback successes and failures. Am J Biofeedback 7:49–58
Levy RA, Jones DR, Carlson EH (1981) Biofeedback rehabilitation of airsick aircrew. Aviat Space
Environ Med 52(2):118–121
Miller NE (1969) Learning visceral and glandular responses. Science 163:434–445
Reason JT, Brand JJ (1975) Motion sickness. Academic Press, New York, NY
Stern RM, Hu S, Vasey MW, Koch KL (1989) Adaption to vection-induced symptoms of motion
sickness. Aviat Space Environ Med 60:566–572
Stern RM, Hu S, Anderson RB, Leibowoitz HW, Koch KL (1990) The effects of fixation and
restricted visual field on vection-induced motion sickness. Aviat Space Environ Med
61:712–715
Yang T, Pei J (1991) Motion sickness severity under interaction of vection and head movements.
Aviat Space Environ Med 62:141
Chapter 14
Overview of the Uses
of Cognitive-Behavioural Training
Abstract I am sure that you will have already concluded that I am very much a
psychophysiologist at heart and that my approach to the solution of a problem lies
in dealing with the whole person; no doubt that is another reason why I am teaching
‘Human Factors Engineering’. So the contents of this last chapter will come as no
surprise. I believe most strongly that many, if not most, stressors can best be dealt
with by using the various component techniques that lie within the
cognitive-behavioural training concept that I have described. I am equally sure that
many of you, if you so desire, will find that you will be as successful as I have been,
or more so, in dealing with a wide variety of psychophysiological problems. In this
last chapter, I shall sum up briefly and in addition, I propose to describe some of my
experiences with these techniques other than in the realm of motion sickness. You
will find that I have used many of my cognitive-behavioural training strategies quite
successfully during sessions of high altitude decompression training at altitude in a
decompression chamber, as well as in a clinical setting, while performing coronary
arteriography and implanting cardiac pacemakers. I have also included some
information from a different field on a relatively recent neurophysiological
approach, which others have described, for the management of tinnitus. I am sure
that you will be interested to note the similarity with my motion sickness prevention
training programme.
Information regarding “motion sickness—a motion adaptation syndrome”, is continually evolving as research efforts progress. Although writings on this subject can
be found as far back as Greek mythology, there is much still to be learned, despite
all the efforts that have gone into this research. Even today, there is no firm
consensus on the aetiology of this syndrome, as I have already recounted. Similarly,
there has been little progress in providing new, effective anti-motion sickness
medications. Nevertheless, the situation is certainly by no means hopeless.
Although there are many holes in our knowledge, there is much that can and is
being done to help those who suffer from this debilitating condition.
© Springer Nature Switzerland AG 2019
T. G. Dobie, Motion Sickness, Springer Series on Naval Architecture,
Marine Engineering, Shipbuilding and Shipping 6,
https://doi.org/10.1007/978-3-319-97493-4_14
295
296
14.1
14
Overview of the Uses of Cognitive-Behavioural Training
Motion Sickness
Motion sickness is a very common and uncomfortable response to provocative
motion environments that also degrades performance. It is a normal protective
mechanism and not a neurotic response. Apart from physiological differences
between individuals, which are difficult to detect, motion sickness involves for the
most part a cognitive overlay based on previous motion experiences and the personality of the individual. I must stress again, however, that this does not mean that
motion sickness is a condition that is “all in the mind.” It is a normal protective
response to which the majority of individuals should be able to adapt. It is particularly unfortunate, however, that many people have become convinced that they
are exquisitely sensitive to provocative motion because of their previous experiences with motion stimulation and the effects that these have had on their ability to
adapt to certain low frequency oscillatory stimuli.
Unfortunately, those medications that are effective in reducing or preventing the
symptoms of motion sickness generally exhibit undesirable side effects. These
unwanted effects are such that the drugs are not suitable for situations in which the
motion-susceptible individual is required to perform skilled tasks or is in control of
potentially dangerous equipment. Cognitive-behavioural training, on the other
hand, is also effective, but carries no such penalty in terms of side effects. This type
of training is relatively time consuming, however, so there is a place for using
suitable medications for passengers or for others in survival situations, where loss
of performance is not a critical issue.
Cognitive-behavioural anti-motion sickness desensitisation training was first
described by myself in the early 1960s when I had desensitised flight trainees, and
later evaluated this technique with my colleagues at the University of New Orleans.
In these studies, beginning in 1989, we focused on answering the various criticisms
that were leveled at the programme in the early days and were able to validate the
need for both of the components in the programme and also to demonstrate its
practicality as a recovery system. Although, as I have stated previously, this
technique appears to involve habituation and adaptation to a particular situation, we
have shown that mere repetitive exposure to provocative motion without counselling has not proven to be beneficial. Since I teach individuals how to handle the
motion response, not just how to adapt to a specific stimulus, this also opens the
door for its use as a means of dealing with a wide variety of stressors. A key
element in the technique appears to be the individual’s ability to learn to control
cognitive focus, thereby blocking out incoming noxious stimuli, while the client
adapts to whatever the stressful environment. Happily, this protection has been
shown to be long lasting and I can see no reason why it should break down once a
person has conquered the problem. As one of my clients has said following his
successful cognitive-behavioural desensitisation training: “Not only do I not get
sick, I don’t even think about getting sick.”
I have applied these counselling procedures successfully to various forms of
motion sickness; such as seasickness, airsickness, car sickness and amusement park
14.1
Motion Sickness
297
ride sickness. In addition, however, the approach may also be beneficial in the
management of a wide variety of incapacitating maladies, such as anxiety and
fainting associated with drawing blood, dental intervention, ophthalmological
procedures, and severe, intractable pain. As you will now see, I have also used the
fundamental elements of this approach successfully to avoid vaso-vagal attacks
during military high altitude decompression training and while performing invasive
cardiac procedures.
14.2
High Altitude Decompression Training
Experienced flight crews undergoing high-altitude pressure breathing training in a
decompression chamber have frequently suffered from vaso-vagal attacks of sufficient severity to cause the decompression chamber training to be aborted. In these
cases the trainees have been considered by others to have failed their training when
they felt faint during the descent following a simulated rapid decompression at high
altitude. I observed that, in these cases, the chamber monitors had all carried out a
similar training routine prior to carrying out the rapid decompression. During the
chamber ascent, the trainees were reminded of the potential hazards associated with
an explosive decompression that had been discussed in detail during their previous
lectures. They were urged to ensure that there was no gas trapped in their gut by
venting it prior to the rapid decompression. The instructor has also emphasised the
need to make sure that the glottis remained open during the decompression so that
the lung gas did not expand within closed lungs. Immediately before a countdown
for the rapid decompression, the monitor again repeated these warnings by asking
each individual if he was quite sure that there were no trapped pockets of gas in the
gut. It was clear that some individuals were not at all sure about this because they
asked for a delay to try to check their bodily comfort. Overall, the team of
supervisors had reported a training failure of 23% due to vaso-vagal attacks associated with that particular training schedule.
I had the opportunity to revise the whole high altitude training programme, with
particular reference to the decompression chamber procedure, along the lines used
in the cognitive component of the cognitive-behavioural anti-motion sickness
training programme. The overall emphasis became entirely positive and the training
scenario was restructured so that the trainees were distracted from the unfamiliar
environment of the decompression chamber. By altering the training approach so
that the subject’s attention has been focused on familiar, real-world occupational
matters during the same rapid decompression scenario, the problem has been
eliminated. Both before and after the simulated decompression, interactive talking
between crewmembers was encouraged in order to simulate the environment of an
operational mission within the aircraft crew compartment.
The restructuring of the training scenario went further than merely altering the
train of events within the decompression chamber, however. Under the old regime,
the rapid decompression was referred to as a “decompression test,” perhaps
298
14
Overview of the Uses of Cognitive-Behavioural Training
implying to some that completing the procedure was indeed a test of their physical
ability to withstand a rapid decompression exposure. I changed this; future trainees
were informed that they had successfully completed their pressure breathing
training (wearing whatever pressure clothing assembly had been appropriate to their
aircraft and operational role). Then, they were told that we now wished to
demonstrate to the crews that their pressure clothing assembly really was as good as
we had stated, by showing them that they would be fully protected following an
emergency decompression at altitude. It was not possible to do this in their aircraft,
but a reasonable simulation could be performed in a training decompression
chamber. This simple alteration alone reduced the intensity of the training procedure; this was now a demonstration of the effectiveness of the equipment and not a
test of their training. The second change has been to paint the door of a room near
the entrance to the decompression chamber the same colour as all the other doors
nearby. Previously, it had been painted red with a white cross on it together with the
words “emergency room.” After all, the instructors knew perfectly well where the
emergency room was located without these embellishments.
When the crews now entered the decompression chamber, they were encouraged
to carry on a fairly continuous routine discussion among themselves concerning the
usual practicalities of a regular flight mission. This was designed to encourage them
to pretend that they were in their aircraft and to report aloud what they would be
doing as part of their crew duties. It was abundantly clear that this distraction
altered the situation significantly. Each member behaved more naturally and entered
into the spirit of the training simulation. In addition, it no doubt helped to prevent
hyperventilation while pressure breathing. It was evident that venting abdominal
gas then occurred as a natural function, as indeed it does in flight. The overall
atmosphere became significantly less tense and the so-called “failure rate” dropped
to zero in the absence of any further vaso-vagal attacks. These changes have been
summarised in Table 14.1. Heightened arousal had been reduced or removed in the
simulated world—in this case, the decompression chamber.
14.3
Cardiac Catheterisation
I have also managed patients on whom I have been performing cardiac catheterisation in like fashion (Dobie 1989). Patients are naturally anxious before undergoing coronary arteriography to investigate the condition of their coronary arteries
or when I have been implanting permanent cardiac pacemakers; both procedures are
carried out under minimal local anesthesia. This is a stressful time for these patients
and the associated arousal manifests itself by a significant rise in heart rate and the
occurrence of frequent extrasystoles. The key to managing this particular situation
also lies in distraction, so that the patient’s attention is directed externally.
Examples of this approach are summarised in Table 14.2.
By treating the procedure as an investigation, which it is, and not a major
surgical procedure, which it is not, the patient’s attitude is altered and he or she
14.3
Cardiac Catheterisation
299
Table 14.1 High altitude decompression training
Positive approach
Negative approach
Referring to the decompression procedure
merely as a “demonstration” to show the
effectiveness of the pressure clothing
Using the term “decompression test” inferring
that the purpose of the decompression
chamber run was a test of the person’s ability
to cope with an emergency rapid
decompression in flight
Environmental hazard reminders—i.e. a red
emergency room door next to the
decompression chamber
Focus on the unfamiliar chamber
environment
Implications:
• Constant reminders of the potential hazards
• Urging to ensure no gas trapped in the gut
• Overemphasizing the need to keep glottis
open during decompression
• No interaction between the crewmembers in
the decompression chamber
Tense, uncommunicative atmosphere
Comfortable environment with no overt
medical hazard reminders (e.g. avoid labeled
E.R. next to decompression chamber)
Focus on real-world occupational matters
Implications:
• Simulation of the environment of an
operational mission within the crew
compartment during decompression training
• Interactive discussions between
crewmembers and monitor regarding their
familiar routine crew procedures in the
aircraft
Relaxed atmosphere regarding routine
mission concerns
Table 14.2 Patient management during cardiac catheterization
Positive approach
Negative approach
Treat it as the clinical investigation that it is
Implications:
• Light meal offered before procedure
• Dentures in
• Walk to lab, or wheel chair if needed for other
physical reasons
Relaxed atmosphere
Always assume patient is alert and listening
Implies major surgical procedure, which it
is not
Implications:
• No meal prior to procedure
• Dentures must be removed
• Transferred to lab on gurney
Tense, uncommunicative atmosphere
Oblivious of patient’s feelings and
reactions
Patient’s attention allowed to focus on
procedure and laboratory surroundings
Focus patient attention away from procedure—
indirectly by means of unrelated distraction
becomes less anxious. It is also important to let the patient know that this procedure
did not necessarily mean that major heart surgery was already a foregone conclusion. Additionally, the attitude of the investigator and the atmosphere surrounding
the study can all diminish the patient’s state of arousal. By focusing their attention
on conversation unrelated to their heart condition, and by directing it away from the
anxiety-provoking atmosphere that can easily arise during such procedures, anxiety
is allayed. Similarly, background music can also have a calming effect on many
patients. Heart rates drop dramatically, minor arrhythmias settle down, and the
patients undergo these procedures more calmly and safely.
300
14.4
14
Overview of the Uses of Cognitive-Behavioural Training
Tinnitus
Tinnitus, or ringing in the ears, may also be noticed as a hissing, roaring, buzzing or
whistling sound in one or both ears. Subjective tinnitus is very common in adults;
affecting approximately 17% of the general population, increasing to around 33% in
the elderly (Jastreboff et al. 1996). This suggests that there could be some 10
million people experiencing tinnitus in the US alone and perhaps 1/5th of these
could be debilitated by the condition. It is interesting to note that Heller and
Bergman (1953) have listed some 29 wide ranging conditions in which tinnitus had
been observed. It is not my intention, however, to even try to discuss these, rather it
is to address the issue of Jastreboff’s neurophysiological approach to managing
tinnitus and draw a parallel with my cognitive-behavioural management of motion
sickness.
Jastreboff et al. (1996) have commented, “It is sobering that there is no cure for
tinnitus, and patients are most frequently advised that nothing can be done …” As a
result of this situation, in the late 1980s Jastreboff proposed his neurophysiological
model of tinnitus and on that basis he developed his form of therapy that included
both a cognitive and a behavioural retraining component (Jastreboff and Hazell
1993). As you will have noted, our two programmes have been born out of
necessity since there had been no satisfactory existing “therapy” available for those
suffering from motion sickness or tinnitus. I propose to quote a description of
Jastreboff’s programme from Jastreboff and Hazel (1993) and you will see the
strong similarity in our two methods.
In the words of Jastreboff and Hazel:
The primary element of therapy is to provide the patient with the understanding of what
causes their tinnitus. Therefore, directive counselling plays a vital role in each case. The
physiology of the auditory system is explained to the patient, with a detailed explanation of
the mechanism of tinnitus that is most probably acting in his/her case. In nearly all cases of
tinnitus the patient feels threatened by the tinnitus. It is important to identify these specific
anxieties about tinnitus, to retrain thinking and to present tinnitus as a benign and harmless
phenomenon, which can be reduced and sometimes eradicated by appropriate treatment. At
the very least we find it is possible to significantly reduce distress evoked by tinnitus. When
patients first visit us they are often very depressed, anxious, alarmed and fixed in their belief
that nothing can be done about their tinnitus. Even if others have been helped, they are
unique in their position of being unhelpable. They are terrified that their problem will be
labeled ‘psychological.’ Strongly held beliefs take time to change and adequate discussion
time (never less than one hour, and often more than two) must be allowed to start the
process of changing these beliefs. In addition, appropriate sequential reinforcement is
needed so that these new ideas can first be understood, and then used to replace the original
inappropriate feelings about tinnitus that caused distress. Typically four to six visits may be
needed over an 18-month period. Only professionals perceived by the patient to understand
the ear and the auditory system are effective in this early stage of directive counseling.
The only significant differences seem to lie in the time frames and number of
sessions; and perhaps the question of using “professional counsellors.” In my case,
the individual sessions are shorter as is the overall length of the programme and I
employ more than 10 sessions in the space of a month. In terms of success, these
14.4
Tinnitus
301
workers have a success rate around 80%, but I have no information at this time on
their long-term follow-up. These apparent differences are small. I am sure that you
will agree that there is a remarkable similarity in our approaches to the management
of these different conditions.
14.5
Theoretical Considerations
These are only three examples of many other areas that can benefit from the
counselling component of the cognitive-behavioural approach, which is designed to
reduce tension and improve a person’s ability to perform more efficiently in
stressful situations. The reduction or elimination of nausea and vomiting caused by
factors other than motion would seem likely goals for this technique, and it may be
possible to train individuals to handle potential mental overload generally. By
properly adapting operational training, subjects can be taught how to handle
unfamiliar environmental distractions that otherwise would degrade their task
performance.
Motion sickness is a distressing problem and, unfortunately, when people are
labeled as being susceptible to it, they believe that there is no hope for them. This
can ruin both their professional and social lives, and increase the already existing
trepidation with which they view provocative motion.
Cognitive-behavioural desensitisation training is a robust technique that can help
most individuals change their attitude toward various forms of provocative motion
that they may encounter. They no longer need to feel that they are “different” or
somehow inferior to those who do not share their “affliction.” It is not a disease, it is
a normal protective response brought about by an abnormal environment. As many
people in all walks of life and in many different occupations have already learned,
susceptibility to motion sickness is not a hopeless situation. On the contrary, given
time and motivation, almost anyone can overcome motion sickness and calmly and
confidently face the most daunting forms of provocative motion, whether on land,
sea, or in the air. As thousands have already discovered, motion sickness can be
defeated.
14.6
Summary
• There is no consensus as to the aetiology of motion sickness, nor have effective
anti-motion sickness medications without side effects been produced.
• Whatever the aetiology of motion sickness, it includes a cognitive overlay based
on previous motion experiences and the personality of the individual.
• Cognitive-behavioural training is a robust technique that instills a true belief that
the individual can tolerate stressful situations and can help him or her to do so.
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Overview of the Uses of Cognitive-Behavioural Training
• Cognitive-behavioural training can be used to ameliorate the effects of
provocative motion and is particularly suitable for those who are operating
potentially hazardous equipment or performing skilled tasks.
• Various aspects of the cognitive-behavioural training concept can be used
successfully to manage a wide variety of stressors.
References
Dobie TG (1989) Teaching the right stuff—the heart of the matter. Aviat Space Environ Med
60:195–196
Jastreboff PF, Hazell JWP (1993) A neurological approach to tinnitus: clinical implications. Br J
Audiol 27:7–17
Jastreboff PF, Gray WC, Gold SL (1996) Neurophysiological approach to tinnitus patients. Am J
Otol 17:236–240
Heller MF, Bergman M (1953) Tinnitus aurium in normally hearing persons. Ann Otol 62:73–83
Uncited References
Brown WH (1916) The mechanism of movement and the duration of the effect of stimulation in
the leaves of Dionaea. Am J Bot III(3):68–90
Darwin C (1875) Insectivorous plants. Appleton and Company, New York
Graybiel A (1964) Vestibular sickness and some of its implications for space flight. In: Fields W,
Alford BR (eds) Neurological aspects of auditory and vestibular disorders. Charles C. Thomas,
Springfield, IL
Guedry FE (1965a) Psychophysiological studies of vestibular function. In: Neff WD
(ed) Contributions to sensory physiology. Academic Press, New York, NY
Kennedy RS, Odenheimer RC, Baltzley DR, Dunlap WP, Wood CD (1990c) Differential effects of
scopolamine and amphetamine on microcomputer-based performance tests. Aviat Space
Environ Med 61:615–621
S.S. 155 (1965) Medical Research Council, Royal Naval Personnel Research Committee