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Secondary Etiological Factors in the Causation of Motion Sickness WALTER H. JOHNSON University of Toronto SUMMARY It is well known that there are great variations in susceptibility to motion sickness; however, much remains to be determined as to the physiologic and psychologic reasons for such differences. Although individual differences in sensitivity of the nonauditory labyrinth undoubtedly constitute the primary factor involved, extralabyrinthine influences constitute secondary etiologic factors of importance under certain circumstances. Vision, cerebral activity, olfaction, food, ambient air temperature, sexual differences, age, and chemical toxicity including alcohol, illness, and adaptation are discussed in relation to their influence on motion-sickness susceptibility. INTRODUCTION As stated by Tyler and Bard (ref. 1), "Motion sickness is a specific disorder which is evoked in susceptible individuals and animals when they are subjected to movements which have certain characteristics." Although it is well known that there are great variations among individuals in susceptibility to motion sickness, little is known as to the physio- logic and psychologic reasons for such differences. As Tyler and Bard again so aptly concluded, "By way of summary about all that can be said is that susceptibility appears to depend on a rather specific constitutional capacity to respond to certain patterns of vestibular stimulation and thus it can be modified to some extent by several extralabyrinthine influences." This last statement was made in 1949, and today, 19 years later, there still remains a dearth of knowledge as to just what these extralaby- rinthine factors are, and this is largely because of lack of significant controlled documentation. When discussing the basic cause of variations in motion-sickness susceptibility under different conditions, it becomes difficult to separate the primary from secondary influencing factors, and the distinction between the two is hard to define. VISION A number of authors have attributed motion sickness to conflicting central effects brought on by conflicting visual, vestibular, and kinesthetic impressions. Sjoberg (ref. 2) noted that suscep- tibility to motion sickness is diminished when the eyes are closed. According to Desnoes (ref. 3), persons watching foam-crested waves or currents in the ship's wake are more likely to become sea- sick, vision here being considered only as a contributing factor. The "witch's house," sometimes seen in amuse- ment parks in which the walls and floor move in- dependently of each other, results in confusion as to orientation in space (ref. 4); that is, there are conflicting impressions between one's field of vision and the remaining equilibrium senses, with resulting nausea and vomiting. Such con- flict, it is said, can also produce nausea without movement of the subject (e.g., when a darkened floor is slanted but the visible walls are set normally). It is a common experience among viewers of wide-screen motion pictures to experience nausea. This is especially effective when highly realis- tic sequences, such as bobsled runs and flight by low flying aircraft, are viewed. Similar ef-
84 THE ROLE OF THE VESTIBULAR ORGANS IN SPACE EXPLORATION fects have been reported in theater presentations of ships at sea (ref. 5). A most interesting correlation between motion- sickness susceptibility and nausea induced by moving visual fields has been reported by Cramp- ton and Young (ref. 6), who concluded, "Indi- viduals susceptible to motion sickness are also sus- ceptible to nausea in a rotary visual field situation, and conversely, nonsusceptibles are resistant." Graybiel (ref. 7) and his associates have made the significant finding that moving visual fields do not cause sickness in the absence of a normal functioning vestibular system; this was estab- lished by exposing labyrinthine-defective humans to appropriate conditions, both in the laboratory and in aircraft aerobatics. The significance of this finding possibly merits further investigation, but it does suggest that moving visual fields cause sickness either by stimulating the vestibu- lar system directly or through evoked head move- ments. Another possibility has been suggested by K. E. Money ("Motion Sickness," Physiol. Rev., in press) who stated â It seems likely that vision modifies vestibular responses nor- mally, in the sense that olfaction modifies salivation, and it may be that a visual stimulus which is normally associated with a vestibular stimulus would give rise to a central vestibu- lar activity in the absence of the vestibular stimulus. This then could explain how moving visual fields cause sickness, since the subjects would not be adapted to the vestibular activity provoked, and it would explain why labyrinthine- defective subjects are immune to such visual stimuli. Vision, however, is not essential to motion sick- ness since blind subjects are susceptible. It is significant to note that, in some circum- stances, vision promotes sickness and in other conditions it suppresses sickness. In the latter case it may be that vision results in diminished vestibular stimulation by acting to control head movements. Several authors (including Kottenhoff and Lin- dahl, ref. 8) have reported the nauseating effect of wearing spectacles that invert the visual field, especially when accompanied by some kind of motion, even walking. It is also known that disturbances such as refractive error or diplopia can cause nausea. No matter what the conditions may be. then, it can be concluded that vision does influence sus- ceptibility to motion sickness, either by increas- ing or decreasing its incidence and severity. Available evidence suggests: In humans visual information which is in agreement with information from the vestibular and other sensory receptors suppresses motion sickness, but only when the circumstances are such that the visual information can influence head move- ments. On the other hand, visual information which is not in agreement with information from the vestibular and other sensory receptors promotes motion sickness (K. E. Money, "Motion Sickness." in press). CEREBRAL FACTORS The outstanding neurosurgicaJ work carried out by Tyler and Bard (ref. 1) showed that the motion-sickness syndrome can occur in decere- brate dogs, the nodulus and uvula of the cere- bellum being the essential components of the central nervous system involved. Removal of the cortex resulted in essentially the same conclusions. It could easily be concluded that no function dependent upon the cerebrum is necessary for motion sickness. However, there is ample evi- dence for believing that the cerebrum does exert considerable control over the brainstem con- cerned, with resulting suppression, on the one hand, or facilitation, on the other. Correia and Guedry (ref. 9) have recently shown that the na- ture of concomitant mental activity strongly affects the development of motion sickness; distracting unrelated tasks such as mental arith- metic have an inhibitory effect while closely associated cerebration facilitates its development. Although anxiety and fear can induce nausea and vomiting, the consensus as the result of con- trolled experiments is that anxiety is not an influencing factor as reported by Graybiel (ref. 7) and probably does not promote its develop- ment very much. It has been reported that the incidence of motion sickness in aircrew is about five times higher during training than during combat (ref. 10). Wendt (ref. 11) has made a particularly excel- lent study of psychological factors in relation to motion-sickness susceptibility and has con- cluded that although suggestion and conditioning do have some effects, "physical and physio- logical factors outweigh them in practical im- portance." He concluded that emotional states and personality defects have no important in flu-
SECONDARY FACTORS IN CAUSATION OF MOTION SICKNESS 85 ence on the development of motion sickness. There is even a report of a decorticate man who exhibited facial pallor and vomiting during a turbulent aircraft flight (ref. 12). OLFACTION The effects of odors, insofar as bringing on the objective signs of motion sickness more readily, are, in a sense, confusing or perhaps surprising. It seems reasonable that odors that are normally considered as being unpleasant would precipitate the classical symptoms more readily than would be the case in their absence, the smell of vomitus being particularly effective. Odors like that of tobacco smoke, however, and even those of food which normally are considered pleasant ones, become the very opposite when some degree of motion sickness prevails; thus, they can be con- sidered in this sense as contributing toward increased susceptibility. FOOD There are conflicting reports as to eating habits in inducing motion sickness. Manning and Stew- art (ref. 13), for example, reported no relation- ship between susceptibility and time duration since eating the last meal, although Fields (ref. 14) reported a relationship, with susceptibility increasing with postmealtime. It is perhaps not surprising, therefore, that student pilots are given conflicting advice by their instructors in this regard. It may well be that the presence of food in the stomach can initiate a gastric aware- ness, especially during aircraft maneuvers in- volving positive g-forces, thereby contributing to a threshold stimulus causing vomiting. Traction on the mesentery during abdominal surgery has been reported to induce nausea (ref. 15) by stimu- lating visceral afferent nerves. A pertinent finding was reported by Johnson (ref. 16) when monkeys were made to regurgitate their stomach contents as the result of being exposed to quickly applied negative g-forces on a centrifuge. Simi- lar experiences have been reported by pilots as the result of so-called Bunting aircraft maneuvers with resulting projectile expulsion of the gastric contents, but without any accompanying nausea. This response cannot be considered as true mo- tion sickness, but it may well account for the difference of opinion that exists as to food in the stomach and susceptibility to motion sickness. AMBIENT AIR TEMPERATURE Uncomfortable heat has been considered to be a contributing factor (ref. 17), and sufferers are known to express a desire for cool fresh air. There is, however, insufficient evidence to sub- stantiate a correlation between ambient air temperature and motion sickness susceptibility. DIFFERENCES BETWEEN SEXES As the result of recording the incidence of airsickness among airline passengers, Lederer (ref. 18), Reason (ref. 19), Hanada (ref. 20), and others have reported that women were more susceptible than men. Why this should be so is unknown, although a feeling of malaise during menstruation is possibly a contributing factor. There is no physiologic reason to believe that vestibular end-organ sensitivity is different between sexes, although endocrine changes may well affect the sensory and associated autonomic responses. AGE There is really no conclusive evidence to indicate any correlation between age and sen- sitivity to motion sickness, although it has been stated that infants and elderly persons are less susceptible (ref. 21). One should remember, however, that infants and elderly people are less active, and hence any nausea-inducing stimulus becomes less intense. Infants spend much of their time either supine or with the head well supported, conditions that render them less vulnerable (ref. 22). It is significant to note that vestibular responses can be demonstrated in infants within a few days after birth. CHEMICAL Although there may be two distinct nausea centers in the central nervous system which are triggered by different means ânamely, chemical stimulus and motion âthere is interdependence between these zones for the production of sick-
86 THE ROLE OF THE VESTIBULAR ORGANS IN SPACE EXPLORATION ness caused by motion. Wang and Chinn (ref. 23) showed that motion sickness required the integrity of both centers even though an emetic drug (apomorphine) required only one of these for its action, the chemoceptive trigger zone that is located in the superficial region of the floor of the fourth ventricle. It may be, as suggested by Chinn and Smith (ref. 10), that motion-sickness vomiting is triggered by "a chemical elaborated in significant amounts during motion." It is not surprising, then, to find that nauseating chemicals lower the resistance to motion sickness. In the case of alcohol, there is undoubtedly a twofold effect that makes it particularly haz- ardous. First of all, it has been established that when the blood alcohol level reaches a significant amount, the threshold for stimulation of the ves- tibular receptors is significantly lowered, so that it readily responds to weaker stimulation. Also, the response to a normally effective stimulus lasts for a much longer period of time. These responses become further complex because of the fact that even in the absence of motion, the subject may experience marked subjective vertigo in certain head positions, a condition that has been called positional alcohol nystagmus (P AN). The initial onset of PAN has been called phase I by Aschan (ref. 24); in man this can be followed several hours later by phase II in which the vertigo and nystagmus return, but occur in the opposite direction, even when all traces of alcohol have left the blood. These effects have been considered as being central in origin, but because the peripheral vestibular receptors are essential at least for the nystagmus, the possi- bility remains that the effect may be on the end organ. In any case, the result is an increased sensitivity to nausea-inducing motion. An additional effect that undoubtedly summates with such increased vestibular sensitivity comes from the effect of alcohol's inducing nausea and vomiting even in the absence of motion. These effects of alcohol can thus add up to a vicious long-lasting combination causing greatly increased sensitivity, the degree of which is dependent upon both the amount of alcohol involved and the subject's sensitivity to alcohol and motion. ILLNESS Certain pathologic disorders undoubtedly have effects similar to alcohol in changing sensi- tivity to motion sickness, although there is a scarcity of any pertinent measurements of this. Women are thought to be more susceptible to airsickness during the menstrual period, but one hesitates to call this an illness. Certain toxemia conditions, as occur with jaundice, kidney dis- ease, and diabetes, can result in nausea and vertigo. Also, toxins produced by foreign bodies such as virus, bacteria, or allergens undoubtedly have both central and peripheral effects that alter susceptibility to motion sickness. Two well-known disorders involving the ves- tibular system are Meniere's disease and ves- tibular neuronitis. Both are characterized by episodes of vertigo, sometimes accompanied by nausea and vomiting in spite of the fact that the involved labyrinth usually shows a hypoactive response to caloric stimulation. It would be interesting, therefore, to determine the sensi- tivity of such patients to motion sickness. It may well be that their threshold might be raised by decreased vestibular sensitivity, although the very opposite could be the case for psychogenic or other reasons. The author is unaware of any significant experiments on this. Vertigo and nausea can, of course, be caused by many other pathologic changes that may well render the subject more susceptible to motion sickness, not only because of the above-mentioned factors, but also because of poor compensatory head responses resulting from lack of interest in the environment. On the other hand, if suffi- ciently ill, the subject may well assume a supine position, which in itself can result in a diminished vestibular stimulation; this is caused by de- creased concomitant head movements or by the fact that the otolith receptors or even canals are in a less vulnerable position. ADAPTATION This author will not discuss adaptation in any detail because it has been well documented and studied by others. In fact, the most meritorious study on this subject has been carried out at Pensacola by Graybiel and his associates in the
SECONDARY FACTORS IN CAUSATION OF MOTION SICKNESS 87 slow rotation room. Adaptation should be men- tioned, however, for the sake of completeness, as a factor affecting susceptibility to motion sickness, although it perhaps should be classi- fied as a primary rather than a secondary factor in this regard. There is no doubt that this phe- nomenon can effectively moderate the physiologic response to nauseating motion in most people. However, the physiologic basis for adaptation still awaits clarification, as is also the case for most, if not all, of the factors that have been mentioned. REFERENCES 1. TYLER. D. B.; AND BARD. P.: Motion Sickness. Physiol. Rev., vol. 29, Oct. 1949, pp. 311-369. 2. SJOBERG. A.: Experimentelle Studien iiberden Ausliistmg- mechanismus der Seekrankheit. Ada Oto-Larynpol.. suppl. 14. 1931. pp. 1-136. 3. DESNOES, P. H.: Seasickness. J. Am. Med. Assoc.. vol. 86, 1926, pp. 319-324. 4. VON DIRINGSHOFEN. H.: Medical Guide for Flying Personnel. Translated by V. E. Henderson, Univ. of Toronto Press, 1940. 102 pp. 5. SCHWAB, R. S.: Chronic Seasickness. Ann. Intern. Med., vol. 19. 1943, pp. 28-35. 6. CRAMPTON, G. H.; AND YOUNG, F. A.: The Differential Effects of a Rotary Visual Field on Susceptibles and Nonsusceptibles to Motion Sickness. J. Comp. Physiol. Psychol., vol. 46, 1953, pp. 451-453. 7. GRAYBIEL, A.: Vestibular Sickness and Some of Its Implications for Space Flight. Neurological Aspects of Auditory and Vestibular Disorders, W. S. Fields and B. R. Alford, eds.. Charles C Thomas, 1964, pp. 248-270. 8. KoTTENHOFF, H.: AND LlNDAHL, L. E. H.: Visual and Emotional Factors in Motion Sickness: Preliminary Communication. Percept. Mot. Skills, vol. 8, 1958, pp. 173-174. 9. CORREIA, M. J.; AND GuEDRY, F. E., JR.: Modifications of Vestibular Responses as a Function of Rate of Rotation About an Earth Horizontal Axis. Acta Oto-Laryngol., vol. 62,1967, pp. 297-308. 10. CHINN. H. I.; AND SMITH, P. K.: Motion Sickness. Pharmacol. Rev., vol. 7, 1955, pp. 33-82. 11. WENDT. G. R.: Of What Importance Are Psychological Factors in Motion Sickness? J. Aviation Med., vol. 19, 1948, pp. 24-32. 12. Doic, R. K.; WOLF, S.; AND WOLF. H. G.: Study of Gastric Function in a "Decorticate" Man With Gastric Fistula. Gastroenterology, vol. 23. 1953, pp. 40-44. 13. MANNING, G. W.; AND STEWART, W. G.: Effect of Body Position on Incidence of Motion Sickness. J. Appl. Physiol.. vol. 1, 1949, pp. 619-628. 14. FIELDS. W. S.: Induced Motion Sickness in Naval Ratings. Proceedings Conference on Motion Sickness, Report C 739, App. D, National Research Council, Canada, Aug. 1942. 15. McEACHERN, D.: MORTON, G.: AND LEHMAN, P.: Sea- sickness and Other Forms of Motion Sickness. War Med., vol. 2,1942, pp. 410-428. 16. LOWRY, R. H.; AND JOHNSON, W. H.: Pseudo Motion Sickness Due to Sudden Negative "G"; Its Relation to Airsickness. J. Aviation Med., vol. 25, 1954, pp. 103- 106. 17. BRt NER, J. M.: Seasickness in a Destroyer Escort Squad- ron. U.S. Armed Forces Med. J., vol. 6, 1955, pp. 469-490. 18. LEDERER. L. G.: AND KIDERA, G. J.: Passenger Comfort in Commercial Air Travel With Reference to Motion Sickness. Intern. Record Med., vol. 167, 1955, pp. 661-668. 19. REASON, J. T.: An Investigation of Some Factors Con- tributing to Individual Variation in Motion Sickness Susceptibility. Flying Personnel Research Committee Rept. 1277, Ministry of Defence (Air Force Department), London, 1968. 20. HANADA, T.: The Studies on Motion Sickness. J. Oto- Rhino-Laryngol. Soc., Japan, vol. 69,1966, pp. 950-978. 21. HOWLETT, J. G.: Motion Sickness. Can. Med. Assoc. J..vol. 76, 1957, pp. 871-873. 22. JOHNSON, W. H.; STUBBS, R. A.; KELK, G. F.; AND FRANKS, W. R.: Stimulus Required to Produce Motion Sickness. I. Preliminary Report Dealing With Im- portance of Head Movements. J. Aviation Med., vol. 22.1951, pp. 365-374. 23. WANG, S. C.; AND CHINN, H. I.: Experimental Motion Sickness in Dogs. Am. J. Physiol., vol. 178, 1954. pp. 111-116. 24. ASCHAN. (;.: Different Types of Alcohol Nystagmus. Acta Oto-Laryngol.. suppl. 140. 1958. pp. 69-78.
