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The Symptomatology of Motion Sickness JACK E. STEELE 6570th Aerospace Medical Laboratories Wright-Patterson Air Force Base SUMMARY Motion sickness is maladaptation to a dynamic environment. The major symptoms are caused by inadequate and inappropriate vascular and circulatory responses, resulting mainly from inadequate perception (integration and analysis of the pertinent sensory data) of the dynamic environment and consequent misestimation of the nature and degree of the threat involved. INTRODUCTION Motion sickness is essentially maladaptation to a novel inertial environment. The symptoms do not develop inevitably in the presence of motion, nor is motion inevitably present when the symptoms do develop (refs. 1 to 4). Motion- sickness symptoms occur only when there is a malfunction of the victim's orientation-perceiving mechanisms and his motion- and acceleration- compensating mechanisms. This is a complex system involving many subsystems. There are various ways in which it can fail or decompensate, depending on the specific nature of the load placed upon it and the individual variations in ability to handle the load. The orienting system integrates and utilizes information from many sense organs, most notably the vestibular, the visual, and the tactile- proprioceptive-kinesthetic. There is much mu- tual interplay among these subsystems. The main systems utilizing the resulting integrated data are the visual, the musculoskeletal, and the cardiovascular. The system contributes to arousal as an important source of early warning of impending threat (danger of falling, being struck, etc.). It is also monitored for reliability. Both orientation information and an estimate of its reliability are available consciously. Either can warn of impending danger. The term "dis- orientation" refers to the condition in which perceived orientation is incorrect. The term "vertigo" (originally meaning a false sense of rotation) now is used commonly to refer to conscious awareness of a failing or inadequate perception of motion and accelerative forces. Conscious fear is relatively unimportant in motion sickness. Unconscious estimate of the threat is most significant. Adaptation to motion consists mainly of learning to perceive it correctly and to make proper adjustment of antigravity compensatory reflexes, etc., and learning to evaluate the threat properly so that inappro- priate defensive preparatory steps are not taken. Symptoms arise as the result of failure to make adequate compensatory adjustments, as the re- sult of inappropriate or incorrect adjustments and preparations, and as a result of the additional information-processing load imposed by incorrect perceptual data processing and the effort to cor- rect it. Similar symptoms can be produced by bringing about these same conditions in various ways, other than by subjecting the victim to the motions typically associated with motion sickness. The novelty of the environment need not be so great as we might expect. Even return to that most familiar condition, 1 g vertical and zero angular acceleration and total zero velocity, can
90 THE ROLE OF THE VESTIBULAR ORGANS IN SPACE EXPLORATION produce symptoms in one who has been thoroughly adapted to some other, such as a ship, a rotating room, or even that environment produced by the disassociation of the normal relationship between the visual and the vestibular sensory inputs in- duced by wearing inverting or reversing spec- tacles (refs. 1 to 6). Such a condition could be called "still sickness" if we persist in attempting to name the disease by the characteristics of the environment that are contributory to its production. Concepts of diseases lead lives of their own. They evolve. As we learn more about them, originally different diseases may come to be con- sidered as but different manifestations of the same underlying disease process, or a disease may fragment into many as we learn to differ- entiate between basically different entities that had but superficial resemblance. As an illus- tration, I offer a disease from antiquity, the "boat disease." This is not a disease of boats but one caused by riding in boats. In accordance with medical tradition, it was named after the old Greek word for boat, "naus," hence nausea. This disease grew to include similar conditions even when they were not caused by riding in boats. Ultimately it lost its status as a disease and reverted to being merely a symptom found as part of many syndromes. We went through the cycle again with seasick- ness which became travel sickness, which then fragmented into mountain sickness, trainsick- ness, carsickness, airsickness, etc. With the advent of laboratory interest in the condition, we acquired rotating chair sickness, Coriolis sick- ness, elevator sickness, swing sickness, and even Cinemascope sickness, 2-FH-2 Hoover simulator sickness, and still sickness. Motion sickness provides a pertinent and insightful name for the syndrome occurring under all of these circum- stances. Even though motion is neither a neces- sary nor sufficient cause (and in the case of 2âFH-2 hover simulator sickness can, when properly applied, actually reduce symptom forma- tion, preceding paper by Fred E. Guedry, Jr., "Conflicting Sensory Orientation Cues as a Factor in Motion Sickness"), motion does indicate the general area in which the victims are mal- adapted, whether with regard to their perception of the actual acceleration and motion environ- ment or in the inadequacy of their compensatory physiological adjustments. "Maladaptation to inertial environment" more accurately (though awkwardly) designates the condition whose mani- festations I am to discuss. For whether the subject is moving or not, whether his environs are moving or not, the inadequacy of his adapta- tion to the dynamic aspects of his environment is the one element that distinguishes the sick subject from the unaffected. When examined closely, the borders separating one disease from another, one body malfunction from another, are not sharp. The blackout and unconsciousness that can result from high ac- celeration in the foot-to-head direction might not seem closely related to the usual symptoms of motion sickness. Yet the same symptoms would be felt every time we arose from a supine to an erect posture were it not for the cardiovascular compensatory adjustments that occur. Lesser derangements of these same adjustments can account for symptoms in many cases of motion sickness. The body is a complex system com- prising many interrelated subsystems. Its malfunctions are better understood from this point of view than from attempts to sharply de- marcate disease entities or to overemphasize the role of any one of the subsystems involved. SYSTEMS INVOLVED IN MOTION SICKNESS In motion sickness, the perceptual-sensory sys- tem dealing with inertia and motion, that part of the central nervous system that is alerted by and prepares for response against external threats, the cardiovascular system, and the neuromus- cular system are involved. I offer a partial trac- ing of the vestibular signals as a rationale for dealing with a hypothetical central processor for dynamic inertial information rather than with detailed neural structures involved. The ves- tibular ganglia communicate with 14 specific neural structures having about 2 dozen mutual interconnections. These, in turn, communicate through approximately 120 identified channels to the next level consisting of 44 centers (ref. 7). Thus, going no farther than three steps from the
SYMPTOMATOLOGY OF MOTION SICKNESS 91 sense organ, and without even considering the visual, auditory, proprioceptive, and other inputs, the system becomes quite unwieldy. Sense organs measure certain qualities of their environment and send signals to the central nerv- ous system. To understand the subsequent chain of events, we must distinguish between the transmission of excitation and the transmission of messages. The distinction is particularly im- portant in discussions of the vestibular system in which corresponding semicircular canals send the same message by shifting the intensity of their signals (repetition rate of their pulse outputs) in opposite directions. This is important in under- standing how the reduced sensitivity found in Meniere's syndrome can lead to sensations of rotation, dizziness, and nausea. A reduced pulse output rate conveys the message of rota- tion as surely as does an increased output rate. A man who has recently lost all vestibular input on one side as a result of surgery is receiving from that side zero input pulses (i.e., zero excita- tion), but a message signifying very strong angular and linear acceleration. Analysis of the produc- tion of symptoms in motion sickness is analysis of changes occurring in the body as the result of all incoming messages concerning orientation, acceleration, and motion (or failing to occur in appropriate response to this information). Sensory organs function normally in motion sickness. At least there is no evidence that they are not functioning normally, and indeed it is extremely difficult if not impossible to elicit motion-sickness symptoms in subjects lacking functional inertia-sensitive sense organs. The central processor is usually not working correctly. Perception of acceleration and motion is usually (though not necessarily always) incorrect. Symp- toms arising directly from this malfunction are minimal, consisting mainly of such illusions as a tilting horizon. Failure of correct central interpretation of acceleration and motion data participates in the generation of major symptoms mainly through the inappropriate or inadequate adjustments of the other subsystems that require the information for their proper functioning and through the elicitation of attempts to correct the central perceptual processor. The cardiovascular system is a major partici- pant in symptom generation, first through failure to compensate adequately for acceleration loads placed directly on it, and, second, by its inability to handle the demands placed on it by the circulatory requirements of muscles inappro- priately preparing for emergency action. The neuromuscular system participates by its in- ordinate demands on the circulatory system and manifests the inadequate central integration of inertial data by ataxia, tenseness, and fatigue. The central arousal system (reticular formation?) participates by triggering several alarm re- sponses, including muscle hyperemia and, more appropriately, the reorganization of inertial perception. Many of the symptoms and other observable conditions of motion sickness are overdetermined. There are several causal chains leading to the same effect. Some of the changes observed are part of the problem, some part of the solution, and some are both. A change compensating for one disturbance may aggravate another. Inadequate cerebral circulation is an old theory of motion sickness. It still has much to recom- mend it. There can be no doubt that nausea often accompanies decreasing blood pressure and falling cardiac output from any cause. Whether or not this nausea is secondary to em- barrassed cerebral circulation is less certain. Two items are of cerebral significance in motion sickness. One is the known increased metabolic demands of the brain in arousal states (ref. 8), and the other is the high correlation between susceptibility to motion sickness and unusual lability of cerebral circulation (at least as reflected by central retinal artery changes) under con- ditions of minor longitudinal g-changes on a horizontal swing (ref. 9). There is some experi- mental evidence that cerebral circulation, or at least the quantity of blood in the head, decreases with vestibular stimulation (ref. 10). Decreased spontaneity, increased depression, and headache are mild indications of impaired cerebral function. Compensation for longitudinal acceleration is about the simplest adjustment the vascular sys- tem must make. Yet it is of considerable mag- nitude. For even so simple a change as shifting from the supine to the erect posture, the hydro- static pressure difference introduced between
92 THE ROLE OF THE VESTIBULAR ORGANS IN SPACE EXPLORATION head and foot is greater than the pressure dif- ference that the heart maintains between its input and its output. To remain adequate, this adjustment requires practice and training. Light- headedness accompanies first arising after sev- eral days in bed. Symptoms may be caused simply by vascular compensatory inadequacy in spite of adequate correction data supplied by the central integrater of inertial data. The after- nausea following various types of motion sickness experiments is aggravated by standing, relieved by sitting or reclining. One of the mildest in- puts, from the point of view of sensory stimula- tion, is capable of producing nausea in a few minutes. This is simple rotation in a vertical plane at a frequency of about 15 rpm while in the seated position (ref. 11). Elevator experiments have shown that g-changes at about this fre- quency are most effective in nausea production, though more time is required (ref. 12). Some have attributed this frequency sensitivity of the nausea-producing mechanism to an undiscovered resonance in the sense organs. I feel that this is a highly unlikely explanation, and far more significant is the fact that this is approximately the natural slosh frequency of the blood in the vas- cular system. Near this frequency the blood un- dergoes the greatest displacement, and the great- est compensatory shift in vessel tone is required. In zero-g experiments, in which zero g alter- nates with increased g, the periods of increased g seem most responsible for the symptoms. In one series, subjects either became sick during the preweightless acceleration or they did not be- come sick at all (ref. 13). In another series in which 51 percent of the subjects vomited at one time or another, no one experienced nausea while prone during the accelerations. Two vomited in this position, but this occurred within 20 seconds of starting the maneuver and with no nausea (ref. 14). It appears that for production of nausea under these circumstances, increased loads on the cardiovascular system are of greatest importance. I participated in two such runs. Allowed to lie down during increased g and to float free during zero g, I experienced no symp- toms. On the later run, confined to a seat, I became nauseated and experienced afternausea hours later while standing. The cardiovascular changes considered up to this point could occur in the absence of any dis- orientation or errors in data processing relevant to motion and inertia. Errors in processing inertial information can only make matters worse. Even in that excellent angular overstimuJation situation, Coriolis stimulation, linear-accelera- tion messages cannot be ignored. Angular ac- celeration about any axis not parallel to the direc- tion of linear acceleration implies a change of direction of linear g. Central-nervous-system determination of direction of linear g (vertical) is a complex thing involving several separate in- puts. In general, the short-term information is derived from semicircular-canal inputs, and the long-term information depends on integration of inputs from the otolith and other organs. With a time constant of only a few seconds for blood displacement caused by linear g, compensation, to be adequate, must utilize some of the implied g-change information based on semicircular- canal inputs. Experimental subjects report that they experience changes in linear g. They describe this as being in a climbing or diving spiral. Objective measurements on the same subjects show actual and different physical re- sponses, depending on whether a climb or a dive is being experienced. Some subjects showed slowed and deepened respiration during the dive," and breath holding during the "climb." Neuromuscular Factors To keep the cause-effect steps in proper sequence, I should like to discuss the neuro- muscular changes before returning to more serious cardiovascular problems that occur secondarily to the muscle changes. The simplest neuromuscular effects are directly caused by improper central-nervous-system integration and interpretation of sensory messages dealing with acceleration and motion. The problem is made more difficult by the need to predict the inertial environment in order that intended movements and dynamic postural reflexes may be properly compensated in time to achieve their objectives. Correcting muscle tension after an arm or leg has been deflected by an improperly predicted force is not a satisfactory solution. We are
SYMPTOMATOLOGY OF MOTION SICKNESS 93 usually unaware of these unconscious compensa- tory contributions to our motions, though we may experience them as a heaviness on first emerging after some time in the water, or as a lightness when first dropping a heavy load. Without the correct sensing and utilization of acceleration data, we experience ataxia and clumsiness. This is somewhat inconvenient and potentially danger- ous, but in most motion-sickness situations greater harm is caused by the body's reaction to what is only potentially dangerous. The part of the alarm reaction that prepares the muscles for anticipated strong action in the face of this implied environmental threat contributes greatly to severe motion sickness. Immediate reflex response to acceleration and motion can contribute to tenseness and sub- sequent fatigue. Benson has found that the gastrocnemius and soleus reflexes in man are increased by angular acceleration (ref. 15). There is no compensatory decrease in the opposite leg, merely a lesser increase. This increase in 16 subjects was from 73 percent to 136 percent, always greater in the trailing leg and linearly related to the table velocity before deceleration over a range from 20Â° to 110Â°/sec. The reaction required the presence of a function- ing labyrinth and was apparently mediated by the gamma efferent system, rather than directly via the alpha motoneurons. The monosynaptic reflexes were unaltered. There is indirect evi- dence for the involvement of the extrapyramidal system in motion sickness. Most antihistamine drugs effective in motion sickness are also effective in Parkinsonism, and a surprisingly large number of drugs primarily identified as effective in Parkinsonism have proven effective in motion sickness (ref. 16). The involvement of the system for dynamic postural reflexes seems evident in both cases. The greatest contribution of the neuromuscular system to the generation of motion-sickness symptoms is probably through the part of the alarm reaction that prepares the muscles for vigorous activity. Increase in blood sugar ap- pears to be part of the solution rather than a cause of symptoms (ref. 17; and Fields, Meakins, and MacEachern, cited in ref. 3, p. 1810). Reducing blood sugar by giving insulin increases the symp- toms. Other indications of alarm response are increased blood and urine levels of catechola- mines and 17-hydroxycorticosteroids (ref. 18). These changes also probably do not contribute to symptoms, but rather to their suppression. Sympatholytic drugs increase the symptom for- mation while sympathomimetic drugs tend to reduce symptoms (ref. 19). One phenothiazine derivative that might have been expected to be helpful turned out not to be, but it differed from the effective drugs in being sympatholytic. The most significant preparatory move by far, how- ever, is the diversion of circulating blood to the muscles. It has been shown that muscle volume in- creases in subjects who are becoming motion sick (ref. 10). This volume shift in preparation for exercise is quite sensitive to central neural control. Weber showed an increase in muscle mass as a response to merely thinking about exercise (refs. 20 and 21). Apparently, actually using the muscles tends to counteract some of the bad effects. Physical work and going about one's business tend to reduce the symptoms (ref. 17). Circulatory compensation for the mass of blood diverted to muscles is difficult. Skin blanching can compensate for only part of it (ref. 10). Other organs, mainly the intra-abdominal viscera, must also lose some of their blood supply. Cardiovascular Factors Having described the manner in which muscle preparation for vigorous action can place addi- tional loads on the cardiovascular system, I should like to examine the evidence that such a load does actually occur and that failure to adjust to it correlates highly with development of symptoms. The most severe motion-sickness symptoms seem to be caused by a decrease in circulating blood volume. In motion-susceptible individ- uals, pulse rate decreases, systolic pressure and minute volume decrease (refs. 10, 22, and 23). The common features are indicative of a pre- collapse state. This is indicated primarily by the sharp drop in systolic pressure and minute volumes in spite of increasing peripheral resist- ance of the arterial system. The body's own esti- mate of inadequate circulation is indicated by
94 THE ROLE OF THE VESTIBULAR ORGANS IN SPACE EXPLORATION increased output of antidiuretic hormone (ref. 24). Stimulation of the Vlllth nerve, whether ca- loric, galvanic, or by angular acceleration, causes a fall in blood pressure (ref. 25). This fall in blood pressure can be blocked by cutting the vagus. Stimulation of the peripheral end of the cut vagus produces a similar fall in blood pressure. Lergi- gan, a phenothiazine derivative, can block the blood-pressure fall produced in either of these ways (ref. 19). It is an effective anti-motion- sickness drug. On the other hand, another phenothiazine derivative, chlorpromazine, a potent and specific antiemetic, is ineffective in motion sickness (ref. 26). This is probably be- cause it lowers blood pressure and can, in large doses, cause vascular syncope. Measures that help combat circulatory collapse reduce motion- sickness symptoms. These are tight abdominal belts (ref. 27), anti-g-suits, intravenous dextran solution, and adrenergic drugs (ref. 19; and Enquist, cited in ref. 19). Other conditions that reduce cardiac output, such as cardiac tamponade or sudden congestive heart failure, tend to produce nausea. Reduced cardiac output can produce symptoms in two ways: those secondary to attempts at com- pensation for the condition and those resulting from inadequate compensation. Blanching of skin and abdominal viscera appear to be com- pensatory. There is little evidence of increased acid production in motion sickness, but blanching would reduce mucosal resistance to that acid which is present. As high as 50 percent of chronic seasick subjects show anatomical changes in the gastric mucosa as a result of such irrita- tion (ref. 28). Sweating, which commonly ac- companies the blanching of the skin, could be compensatory for the skin's reduced effectiveness as a cooling organ. Sweating could also be part of the preparation for vigorous muscle action in anticipation of increased heat production. There are no reports on the actual body temperature of motion-sick subjects, though their common desire for cooler surroundings would indicate the im- pairment of heat-loss mechanisms. It is not known for certain how decreased car- diac output and blood pressure produce nausea. There are several reasons to believe that it in- volves embarrassment of cerebral circulation and metabolism. Decreased oxygen tension seems responsible for the nausea of mountain sickness. There is a higher incidence of motion sickness in unpressurized aircraft flying at higher altitudes. Vestibular stimulation has promptly reduced the volume of blood in the brains of dogs and monkeys (ref. 8). Measures that tend to improve cerebral circulation can reduce symp- toms without necessarily improving the general level of cardiac output. Lowering the head, for example, in a maneuver similar to that employed for the prevention of vascular syncope, can re- lieve the nausea (ref. 23). Nausea is less on sitting than on standing, and still less on recb'ning. Subjects with poor regulation of cerebral circu- lation are more susceptible to motion sickness (ref. 9). Retching or vomiting does, at least momentarily, raise the intracranial blood pres- sure. This is the only compensatory value ob- servable for such a reflex, other than removing irritants from the gastrointestinal tract. It is notable that nausea accompanies cerebral circu- latory embarrassment produced by various other causes. CONCLUSION The human body is a very complex system. In attempting to understand some malfunction we should not delve so deeply into one sub- system that we lose sight of the others. Previ- ously, seeking the cause of motion sickness, I have denigrated the role of the sensory systems and emphasized that of the perceptual or central integrative system, but of course without sensory input there is nothing to perceive or integrate (ref. 29). In preparing the present paper on symptomatology, I was impressed by the role of the extrapyramidal and vascular systems. Both Parkinsonism and increased susceptibility to motion sickness have been reported as after- effects of viral encephalitis. A large number of the same drugs are useful in both conditions. Dynamic postural reflexes are increased under conditions of acceleration. Muscle volume also increases. The major symptoms seem to be caused by cardiovascular inadequacy, secondary to diver- sion of circulating blood to the muscles in response to a threatened need for vigorous
SYMPTOMATOLOGY OF MOTION SICKNESS 95 muscular action on the basis of inadequately perceived inertial and dynamic environment. The problem is aggravated in people with poor cerebral circulatory control. Vagotonic subjects are more susceptible. Cholinergic drugs aggra- vate and anticholinergic drugs ameliorate the symptoms. Two of the most effective anti- motion-sickness drugs, scopolamine and amphet- amine, have little else in common except perhaps their usefulness in Parkinsonism. One blocks the vagus-mediated fall in blood pressure and cardiac output. The other increases blood pressure and cardiac output. These effects are additive against motion sickness. A disease that began in the stomach has moved through the ears, the brain, the musculature, the visual, the circulatory, the endocrine, the thermo- regulatory, the urinary, and back to the upper intestine (increased serotonin content). What have we overlooked? REFERENCES 1. BRUNEI). J. M.: Seasickness in a Destroyer Escort Squadron. Armed Forces Med. J., vol. 6, Apr. 1955, pp. 469-490. 2. MILLER, J. W.; AND GOODSON, J. E.: A Note Concerning "Motion Sickness" in the 2-FH-2 Hoover Trainer. Naval School of Aviation Medicine Rept. 519, Pensa- cola, Fla., 1956. 3. MONNIER, D.: Le Mai de Mer; Pathogenie et Traitement. Rev. Pathol. Gen., vol. 56, Dec. 1956, pp. 1800-1830. 4. ANON.: The Concept of Motion Sensitivity. Intern. Record Med., vol. 168, June 1955, pp. 371-376. 5. KOHLER, I.: Experiments With Prolonged Optical Distortions. Presented at XlVth Intern. Congr. Psychol., Montreal, June 1954. 6. 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. 7. RAPOPORT, A.; HORVATH, W. J.: SMALL, R. B.; AND Fox, S. S.: The Mammalian Central Nervous as a Network. AMRL-TR-67-187, Aerospace Medical Research Laboratories, Wright-Patterson Air Force Base, Ohio, 1967. 8. KETY, S. S.: Considerations of the Effects of Pharmaco- logical Agents on the Over-all Circulation and Metabolism of the Brain. Neuropharmacology, H. A. Abramson, ed., Josiah Macy, Jr., Foundation, 1955, pp. 13-89. 9. VAN EGMOND, A. A. J.; GROEN, J. J.; AND DEWIT, G.: Selection of Motion Sickness-Susceptible Individuals. Intern. Record Med., vol. 167, Dec. 1954, pp. 651-660. 10. JOHNSON, W. H.; SUNAHARA, F.; AND TAYLOR, W. J. R.: Some Physiologic Responses to Vestibular Stimulation. Third Symposium on the Role of the Vestibular Organs in Space Exploration, NASA SP-152, 1968, pp. 355- 362. 11. KELLOGG, R. S.: Dynamic Counterrolling of the Eye in Normal Subjects and in Persons With Bilateral Labyrinthine Defects. The Role of the Vestibular Organs in the Exploration of Space, NASA SP-77, 1965, pp. 195-202. 12. ALEXANDER, S. J.: COTZIN, M.; HILL, C. J., JR.; RtcciUTi, E. A.; AND WENDT, G. R.: Studies of Motion Sickness. 1. The Effects of Variation of Time Intervals Between Accelerations Upon Sickness Rates. J. Psychol., vol. 18,1945, pp. 49-62. 13. VON BECKH, J. J.: A Summary of Motion Sickness Experiences in Weightless Flights Conducted by the Aeromedical Field Laboratory. Symposium on Motion Sickness, With Special Reference to Weightlessness, AMRL-TDR-63-25, Aerospace Medical Research Laboratories, Wright-Patterson Air Force Base, Ohio, June 1963, pp. 67-72. 14. LOFTUS, J. P.: Motion Sickness in the C-131 B. Sym- posium on Motion Sickness, With Special Reference to Weightlessness, AMRL-TDR-63-25, Aerospace Medi- cal Research Laboratories, Wright-Patterson Air Force Base, Ohio, June 1963, pp. 3-5. 15. BENSON, A. J.: Effect of Labyrinthine Stimulation on Reflex and Postural Activity in Gastrocnemius Soleus Muscle Group in Man. J. Physiol., vol. 146, 1959, pp. 37-38. 16. CHINN, H. I.: Evaluation of Drugs Effective Against Mo- tion Sickness. USAF School of Aviation Medicine Rept. 55-144, Randolph Air Force Base, Tex., Oct. 1955. 17. HARBERT, F.; AND SCHIFF, M.: Motion Sickness. U.S. Armed Forces Med. J., vol. 1, Sept. 1950, pp. 979-984. 18. COLEHOUR, J. K.; AND GRAYBIEL, A.: Urinary Excretion of Corticosteroids and Catechol Amines in Normal Persons and Deaf Subjects With Bilateral Vestibular Defects Following Acrobatic Flight Stress. Aerospace Med., vol. 35,1964, pp. 370-373. 19. GERNANDT, B. E.; AND SCHMITERLOW, C. G.: Some Observations Concerning the Mode of Action of the Antihistaminic Drug 'Lergigan' (Na-Methyl-/3-dimethyl- Aminoethyl) phenothiazine hydrochloride) in Motion Sickness. Brit. J. Pharmacol., vol. 8, June 1953, pp. 181-186. 20. WEBER, E.: Ueber den Einfluss der Lebensweise und Fortbewegungsart auf die Beziehungen Zwischen Hirnrinde und Blutdruck. Arch. Physiol., suppl., 1906, p. 309.
THE ROLE OF THE VESTIBULAR ORGANS IN SPACE EXPLORATION 21. WEBER, E.: Ueber die Ursache der Blutvershiedbung im Korper bei vershiedenen physichen Zustanden. Arch. Physiol., 1907, p. 293. 22. POWELL, T. J.: Acute Motion Sickness Induced by Angu- lar Acceleration. FPRC Rept. 865, Institute of Avia- tion Medicine, Farnborough, Hants, England, Feb. 1954. 23. BRIANOV, I. I.; DEGTIAREV, B. A.; LAPSHINA, N. A.; KALMYKOVA, N. D.; AND RASKATOVA, S. R.: Hemo- dynamics During Vestibular Stimulation. Voenro- Med. Zh., Moscow, no. 11,1966, pp. 45-50. 24. TAYLOR, N. B. G.; HUNTER, J.; AND JOHNSON, W. H.: Antidiuresis as a Measurement of Laboratory Induced Motion Sickness. Can. J. Biochem. Physiol., vol. 35, 1957, pp. 1017-1027. 25. SPIEGEL, E. A.; AND DEMETRIADES, TH. D.: Contribu- tions to the Study of the Vegetative Nervous System. Part III. The Influence of the Vestibular Apparatus on the Vascular System. Pfliigers Arch. ges. Physiol.. vol. 196. 1922, pp. 185-199. 26. GOODMAN, L.S.; AND GILLMAN, A.: The Pharmacological Basis of Therapeutics. Second ed. Macmillan Co., 1955. 27. POPPEN, J. R.: Seasickness: Etiology and Treatment. U.S. Naval Med. Bull., vol. 37, July 1939, pp. 463-469. 28. SCHWAB, R. S.: Chronic Seasickness: Neurological. Psychiatric, and Naval Aspects. U.S. Naval Med. Bull., vol. 40, Oct. 1942, pp. 923-936. 29. STEELE, J. E.: Motion Sickness and Spatial Perception. Symposium on Motion Sickness. With Special Refer- ence to Weightlessness, AMRI.-TDR-63-25, Aero- space Medical Research Laboratories, Wright-Patter- son Air Force Base, Ohio, June 1963, pp. 43-65.
SYMPTOMATOLOGY OF MOTION SICKNESS 97 DISCUSSION FOLLOWING ALL OF SESSION III Whiteside: Dr. Johnson has earned a reputation as being the man who really brought the subject of motion sick- ness onto a rather different level. It was his work in im- mobilizing the head of people who are flying which high- lighted the importance of the factor of head mobility when angular accelerations are present and, therefore, of course, the associated development of the so-called Coriolis effects. There is one big difficulty that we often have in this type of exercise. You cannot really understand the function and the mode of action of many of the symptoms leading up to a syndrome unless you step back and come out of the woods. I think we tend at this stage to be unable to see the trees because we are in the woods. Words like "conflict" and so forth have been mentioned. I personally think that this is a most promising line of approach, and, indeed, it forms the basis of the philosophy which Lieutenant Colonel Steele has toward this subject. I believe he is in effect doing this extremely useful step of taking us back, looking at the assem- bly of symptoms, and trying to interpret them in an integra- tive way. This is what we tend not to do. Inevitably, we must look at the bits and pieces, but we must also try to get an integrative view of this problem and see the integrative action of all these factors as they combine to give rise to this syndrome. Blatt: This may be somewhat anecdotal, but I think it may be pertinent. Parenthetically, one might say that the theme of this meeting today might come from a chapter of the book of the great Greek historian, Herodotus. The name of that book was "Airs, Waters and Places." When I was a corpsman in the Army during World War II, we used to work about that beach in Hawaii where training was being given in landing for beach assault. This beach was next to a sugar mill. It was interesting that whenever the sugarcane was being processed, that is, the grinding occurred, there appeared to be an increase in the frequency of motion sickness, because of this sickening smell of sugar-cane processing. In southern Louisiana there are many many sugar mills, and grinding starts about the second week of October. It is very interest- ing that, at about that time, there is an increase in frequency of motion sickness in the immediate environment of the sugar mill. The odor of fresh sugar being processed appar- ently can cause this. In addition, some of the employees who are new to the sugar-grinding industry will complain of a sensation of whirling. It is also interesting that one such individual, who, at the beginning of each year of grinding would have a perennial episode of vertigo with nausea in association with this exposure, no longer complained of this after a laryngectomy for malignancy. Of course, this is subjective. Also, it is interesting that, during the month of October in Louisiana, people who go water skiing about the lakes and bayous next to the sugar mills, which are in opera- tion 24 hours a day, also complain of this combination of nausea and vertigo when they are immediately exposed to that kind of environment. Money: I should like to ask Dr. Steele what the evidence is for a blood-sugar increase in motion sickness. I saw one negative report. I am wondering where his positive one was found. Steele: This was reported by Monnier (ref. 3 of text) and by Harbert and Schiff (ref. 17). Incidentally, the increase is not necessarily in motion sickness, but to motion, being a compensatory change. As I did mention, the decrease in blood sugar was reported as augmenting the symptoms, whereas an increase tended to reduce symptoms. Money: That explains the difference, because the negative report I saw compared two groups of subjects both of whom were exposed to motion. When they compared the blood sugar of the sick group to that of the nonsick group, there was no difference. Miller: We have done a number of studies here in Pensa- cola on labyrinthine-defective subjects and have never really had any success in getting them motion sick. Are you sug- gesting that your head-over-heels procedure might elicit motion-sickness symptoms in these individuals? Steele: I really wondered about that. Participants in this experiment at least admitted no symptoms. This would indicate that more of the problem is in the message, in its analysis, and in the adjustments made in response to that information rather than in an adjustment made to the actual displacement of blood. The exposure of 3 minutes is not really what I would consider a severe exposure. 1 wish more effort were made to nauseate these subjects in other ways than by putting stimuli through their nonexistent sensors. The problem of canal sickness is a little like the problem of the retinal disease which is manifested also by nausea and sometimes by fainting; it is well known that blind men do not faint at the sight of blood. But this does not really implicate too greatly the retina. Whiteside: I really am intrigued at the way these factors of conflict keep coming up, perceptual conflict is really what I am referring to, and the way in which adaptation is referred to could be interpreted as adaptation to the conflict situation. To be a little more specific, when the conflict is one involving vision, the eyes are caused to move by a variety of involuntary stimuli, such as the vestibular stimuli which have been con- sidered. One stimulus which has not been considered but which may play an important role is the tonic neck reflex. The eyes inevitably move a small amount as one is observing something, and one gets a visual sensation of movement. Some of that sensation may be suppressed or eliminated by a better control of the eye movement. This control in response to a specific type of deviation of the eyes from the target may well be a factor in the so-called adaptation which seems to take place to a particular type of motion. Control of eye fixation may play a part in the observation that a man becomes adapted to the motion of a specific ship of a certain tonnage and size. He then goes onto a different type of a ship and he becomes seasick once more. Lansberg: My remark and question concern positional alcohol nystagmus and are directed to Dr. Johnson. I have done quite a few of these experiments, and perhaps it has been an unforgivable neglect on my part, but I am afraid I
98 THE ROLE OF THE VESTIBULAR ORGANS IN SPACE EXPLORATION did not notice much nausea. The subjects got nystagmus, but they did not get nausea or vertigo concurrent with ihe nystagmus. Is that right, or did I understand that you meant to say that vertigo accompanies the positional alcohol nystag- mus, or do you feel th.it vertigo and positional alcohol nystag- mus are quite separate? Johnson: I did not mean to say that the positional alcohol nystagmus causes nausea, although we all know that nausea can result from too much alcohol. We know, however, that such nystagmus is dependent upon the presence of the vestibular end organ. Lansberg: That is right. Stone: Dr. Miller, in the seat rotation tests where the subject moved his head or body, did you measure the rate of motion of the head in these situations? If you did. as the rate of the chair was increased did the subjects tend to reduce the rate of their head and body motions? Miller: The velocity of the chair was held constant in any given test. The rate of head (body) motion was always essentially the same and independent of chair velocity- it was controlled by having the subject follow taped in- structions which provided the temporal sequence as well as the direction of each head tilt. Monitoring by the experi- menter further assured that the subject tilted his head approximately 90Â° and at the proper rate; i.e., 1 second to the tilted position, 1 second return to upright. Occasionally we have found that a subject might tend to restrict the magni- tude of his head movements when he began to develop symptoms, but he was quickly admonished about this and always required to follow the standard procedure.
SESSION IV Chairman: E. J. Baldes U.S. Army Aeromedical Research Laboratory