Transportation Research Record 1059 75

Review of Motion Sickness with Special Reference to Simulator Sickness

R. S. KENNEDY and L. H. FRANK

ABSTRACT

simulator sickness has implications for training and safety because as many incidents of simulator sickness have been reported since 1980 as in all the previous time. The signs and symptoms, stimulus and response characteristics, anatomical structures, and susceptibility factors of simulator sickness are reviewed. The prevalent theories of the genesis of this malady are put forth and an integrating theory, which suggests that simulator sickness is a form of motion sickness and may be best understood as a special case of sensory con­ flict, is proposed. Sensory conflict is a useful principle in the study of sim­ ulator sickness because the malady is clearly polygenic and polysymptomatic. Therefore it may be argued that greater conflict leads to more severe and greater incidence of sickness. Evaluations that will lead to recommendations for preventing the problem, guidelines for predicting the outcome, and sugges­ tions for future research may be planned.

Simulator sickness is not a new phenomenon for those history of motion sickness began with man's domesti­ who have worked around training devices and other cation of animals for transport. Riding camels or optical devices that have dynamic character is tics. elephants, for example, can induce motion sickness i Moreover, to those who have experimented with per­ but, interestingly, riding horses does not (5). With ceptual adaptation to optical transformations, it is the invention of the boat came seasickness -and the not surprising that sickness . occurs. For those who question of whether a seaman could perform his perform experiments in vestibular science, simulator duties. In short, motion sickness became operation­ sickness may be considered the visual analogue of ally significant. Thus the search for the causal more traditional forms of motion sickness, including factor or factors of motion sickness probably re­ space sickness (1). ceived its initial impetus from a practical concern Simulator sickness, although not necessarily of about how to eliminate its debilitating effects. epidemic proportions, is on the upswing. Almost as many incidents have been reported since 1980 as in all the years before then. A sourcebook (~) reports many relationships among causal factors, and a work­ MOTI~N SICKNESS--A DEFINITION shop has been held to discuss the implications of simulator sickness (}). Simulator usage is also in­ Motion sickness is a general term for a constella­ creasing, and there is a question about whether the tion of symptoms and signs, generally adverse, caused by exposure to abrupt, periodic, or unnatural ac­ increase in observed frequency is due to the in­ celerations. Overt manifestations (signs) are pallor, creased availability of simulators, increased kine­ sweating, salivation, and vomiting (12-15). Drowsi­ matics available in simulated scenarios, or even ness, dizziness, and nausea are the chief symptoms. individual differences of today's user population. Less frequently repor·ted, but often present, are There have been five major (and many minor) re­ views of the motion sickness literature and postural changes, or ataxia, sometimes referred to all of these contain excellent accounts of what is as "leans" or "staggers" (16,17). Other signs (5,18, known. Each has a comprehensive reference list. The _!i) include changes in cardi~ascular, respiratory, following review has been prepared to emphasize the gastrointestinal, biochemical, and temperature regu­ authors' bias that, as is the case with other forms lation functions. Other symptoms include general of motion sickness [e.g., space adaptation syndrome discomfort, apathy, dejection, headache, stomach (!,,2_-11)], simulator sickness may be best understood awareness, disorientation, lack of appetite, desire in the context of motion sickness as a special case for fresh air, weakness, fatigue, confusion, and, of sensory rearrangement. occasionally, incapacitation. The consequences for human performance and operational efficiency are decreased spontaneity, carelessness, and incoordina­ INTRODUCTION tion, particularly in manual control. Motion sickness is theoretically preventable, but that is not always practical. When symptoms are severe, the passage of Although the self-propelled locomotive behavior of man (walking, running, jumping) does not induce mo­ time may be the only possible treatment. tion sickness, transportation in some environments does. It is probably reasonable to assume that the STIMULUS CHARACTERISTICS R.S. Kennedy, Essex Corporation, 1040 Woodcock Road, Orlando, Fla. 32803. L.H. Frank, Virginia Polytech­ Many types of motion produce motion sickness. Among nic Institute and State University, Blacksburg, Va. the most common places for sickness to occur are in 24061. ships, small boats, trains, gliders, zero-gravity 76 Transportation Research Record 1059 aircraft, rotating rooms, chairs, vertical oscil­ TABLE 1 Physiological Manifestations of Motion Sickness• ( 11) lators, horizontal swings, and moving-base or fixed­ based flight simulators. In addition, tilted rooms Manifestation and buildings and chimneys have been implicated. Humans appear to be most susceptible to motion Cardiovascular Changes in pulse rate or blood pressure, or both lttcreaseu lune of ai lelial pm lion of capillaries i11 lit~ sickness when exposed to very low frequency vibra­ fingernail bed tions in the range of 0.12 to 0.25 Hz (20), although becreased diameter of retinal vessels the data are limited largely to those from swings Decreased peripheral circulation, especially in the skin of and vertical oscillators. There does not appear to the head be a frequency-specific relationship when cross­ Increased muscle blood flow Rcspiiatory Alterations in respiration rate coupled angular accelerations are employed (21) . The Sighing or yawning normal locomotive behavior of man has a mean fre­ Air swallowing quency of about 1. 7 Hz (~,ll) and, as previously Gastrointestinal Inhibition of gastric intestinal tone and secretions mentioned, does not induce sickness. Salivation Most of the power used in spectral density analy­ Gas or belching Epigastric discomfort or awareness ses of body sway is below 0.40 Hz (±_!), and perhaps Sudden relief from symptoms after vomiting platform stimuli in this range could be amplified at Body fluids Changes in lactic dehydrogen ASE concentrations the head. Although acceleration of the environment Blood Increased hemoglobin concentration is generally required, visual perception of motion Increased pH and decreased paC02 levels in arterial alone is sufficient to produce sickness (25,26). The blood, presumably from hyperventilation effects are usually limited to the period of expo­ Decreased concentration of eosinophils Increased 1 7 -hydroxycorticosteroids sure, but "postadaptation" effects are known to occur Increased plasma proteins

ANATOMICAL STRUCTURES RELATED TO MOTION SICKNESS have examined the evidence for this theory on earth by the use of head-down tilt to induce fluid shift. Table 2 is a list of anatomical structures and their Their work has shown that fluid shift toward the probable role in motion sickness. The interested head has no effect on susceptibility or causes a reader is referred to the longer version of this small decrease in susceptibility as the magnitude of paper (2) or to Money's and wood's (45) excellent the shift increases (41). review ~f the neural mechanisms underlying the symptomatology of motion sickness on which it was based. Individual differences and other factors are FEAR AND ANXIETY THEORY given in Table 3. Does anxiety or fear increase a person's suscepti­ bility to motion sickness? According to Benson (52, TABLE 2 Anatomical Structures Related to Motion p,486), "a definite correlation between susceptibil­ Sickness ity and psychometric measures of anxiety or neuroti­ cism has not been established." It is not known for Structure Role certain whether this is due to a true lack of rela­ tionship or, perhaps, to the lack of reliability in Vestibular apparatus Probably required Visual apparatus Important, not necessary measures of anxiety (53) as well as to the already Viscera Definitely not necessary mentioned lack of reliability in measures of the Proprioceptive afferents Not known motion sickness criterion. In any case, clear-cut Visual afferents Not known evidence for the notion is hard to find. Peripheral afferents Important, may not be necessary Vestibular nuclei Probably necessary Chemoreceptor trigger zone Necessity presently challenged Cerebrum Not necessary BALANCE OF AUTONOMIC ACTIVITY POSTULATE Limbic Speculatively related Waxing and waning of symptoms suggests competing processes (54). The symptoms of motion sickness resemble what might be associated with increased TABLE 3 Individual Differences and Other Factors in Motion cholinergic (~) and decreased adrenergic activity, Sickness but the relationships are not clear-cut (~. Al­ though the drugs which are effective in motion sick­ Findings Factors ness are chiefly those that stimulate the sympathetic Sex Men appear less susceptible nervous system, or those that shut down the parasym­ Age Younger than 18 months-virtually immune pathetic nervous system, the several exceptions (56) 2 years to puberty-high imply that this postulate should be considered as Puberty to 21-decreasing part of a larger theory. 21 to 5 0-declining Older than SO-rapidly disappearing Field independence Appears to be related in several studies Adaptation Repeated exposures invariably result in lessening TOXIC REACTION THEORY of symptoms Head movement In most environments increases the symptoms Treisman <21.l addressed the evolutionary significance Motion regularity The more complex the motion, the more sickness of the emetic response to motion sickness. What, Treisman asked, is the adaptive function of vomiting during motion sickness, and how does such a response There is considerable evidence that overstimula­ contribute to the survival of the species? His answer t ion does not satisfactorily account for all inci­ was that the only adaptive significance vomiting dences of motion sickness. As has been mentioned, could have is the explusion of ingested toxins from vision alone is sufficient to induce sickness as the body. Hence, when the body vomits in response to demonstrated in the case of some fixed-base simula­ motion sickness, it is interpreting the stimulus as tors (46). Motions that are difficult to consider if it were a poison. Wiker (~) has also made this overstimulating, such as slow rotation rooms and point. ship movement, can induce severe sickness. Normally, the sensory systems of the body comple­ ment each other. The eyes and the vestibular system are in harmony. When a toxin is ingested, it acts on the inner ear causing the vestibular signal to come FLUID SHIFT THEORY in conflict with vision and other senses. This con­ flict signals to the body that it has ingested a The idea that fluid shifts within the body may con­ poison and emesis occurs. tribute to motion sickness is both recent (47) and old (48). Wallaston (48) claimed that motion sickness was caused by sloshing of the blood, which led to PERCEPTUAL CONFLICT THEORY alternate engorgement and anemia of the brain. That fluid shift may be a possible explanation of Perceptual conflict theory is known by several names: space motion sickness accounts for the majority of mismatch, neural mismatch, cue conflict, incongruity, research anc interest in fluid shift theory. During and sensory rearrangement. The authors believe that space flight there is a cephalic shift of 1.5 to perceptual conflict is the most descriptive term 2.0 L from the lower extremities (11). Calf girth and, consequently, recommend its use. correspondingly decreases about 30 percent. Mean In brief, the perceptual conflict theory posits a resting heart rate and systolic blood pressure tend referencing function in which motion information, to increase, while diastolic pressure decreases. signaled by the eyes, vestibular apparatus, or pro­ According to space fluid shift theory, the rostral prioception, may be in conflict with expected values shift in body fluid alters cranial pressure and ves­ of these inputs based on a neural store (which re­ tibular response. For example, altered fluid pressure flects past experience) or with the way in which the in the labyrinth could result in a change in gain system circuitry is wired. Kennedy (~) suggested, and phase shift (i2_) • Graybiel and Lackner (~,~) as have others (~ 1 §.Q_) , that perceptual conflict 78 Transportation Research Record 1059 theory is based on a lack of correlation between if the vestibular system is implicated, the system appearance and reality. Under ordinary circumstances, interprets this to mean that the organism has been there is a correspondence between what is sensed and poisoned. Under some conditions, the body possesses the physical representation of the stimulus. The resonances that, in the case of 0. 20 Hz or so, the sensory systems report reality and, after periods of system also interprets as poison. It is wondered time, create a neural store of expectations. The whether 0.20 Hz, or another resonance, would have an expectations are also referenced to the sensory adverse (i.e., it's poison!) effect with visual channel that delivered them and are stronger for stimuli alone. If so, such a finding would have more experiences and also in those ranges within strong heuristic value for simulator sickness. which the channel is most sensitive. The purpose of information processing and perception functions is to predict reality in order that one may interact ACKNOWLEDGMENT with it, spatially and temporally. The authors be­ lieve that central nervous system integration could This study was supported in part by the Naval Train­ be represented by a linear model (61). This version ing Equipment Center. of the sensory conflict theory is described in greater detail in Kennedy and Frank (~) and Kennedy et al. (63). REFERENCES

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