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Prevention of Motion Sickness in the Slow Rotation Room by Incremental Increases in Strength of Stimulus ASHTON GRAYBIEL Naval Aerospace Medical Institute SUMMARY Two groups of experiments in the Pensacola slow rotation room demonstrated the possibility of preventing motion sickness in human subjects by incremental exposures to otherwise highly stressful Coriolis accelerations. These accelerations were generated by motions of the subject's head out of the plane of the room's rotation. In the first experiment, control of the accelerations was maintained principally through regulation of the room's velocity. In the second, the adaptation was speeded up by control over head motions made by the subjects as well as over the room's velocity. The cardinal findings in these experiments have important theoretical and practical implications in adaptation to Coriolis accelerations, as well as in the prevention of motion sickness by "natural" means in a rotating'spacecraft. INTRODUCTION This report deals with experiments in the Pensacola slow rotation room designed to prevent motion sickness by means of incremental increases to otherwise almost intolerable levels of Coriolis accelerations. The primary etiological factor causing slow rotation room (SRR) sickness is stimulation of the vestibular organs, especially the semi- circular canals, by Coriolis accelerations generated by rotations of the subject's head out of the plane of the room's rotation. Thus, control of the stressor is exercised through regula- tion of the room's angular velocity, which is accomplished accurately and without difficulty, and control over head rotations, which is not so readily accomplished in the active subject. With regard to the latter, the experimenter exercises control by requesting the subject either to fixate his head, to carry out tasks in- volving stressful head rotation, or to execute standardized head motions. With head fixed, the stressor is "off"; adaptative processes come to a halt, and if motion is present, the oppor- tunity for restoration is initiated. When assigned tasks of a general nature are carried out, it is difficult to measure the incidental stressful head motions involved. Only if the head motions are standardized and precisely carried out are quantitative data obtainable; obviously, however, the experimenter has only limited control over head motions even when subjects cooperate fully. Subjects left to their own devices differ in the number of stressful head rotations made whether or not motion sickness is present. The experiments to be described fall into two groups. In the first, control of the stress was exercised mainly through regulation of the SRR angular velocity; and in the second, con- trol over the subjects' head motions as well as the room's velocity was attempted. A terminal velocity of 10 rpm was chosen partly because of the small likelihood that rotating orbiting spacecraft would exceed this velocity and partly because, in our experience, normal subjects suddenly exposed in a room rotating at 10 rpm invariably became sick while carrying out assigned tasks and housekeeping activities (refs. 1 to 4). Under different conditions, how- 109
no THE ROLE OF THE VESTIBULAR ORGANS IN SPACE EXPLORATION ever, susceptibility to motion sickness at rota- tional velocities of 10 rpm may not be so great (refs. 5 to 7). ADAPTATION THROUGH CONTROL OVER VELOCITY OF THE SRR Three initial probes were unsuccessful (ref. 8). Two involved three incremental steps to terminal velocity on the SRR (10 rpm) over a period of approximately 3 days, and the third a series of 40 incremental steps over a period of 40 hours. The subjects were free to follow their own interests except during testing periods of 4 hours in the morning and afternoon. Although all of the subjects experienced motion sickness, it was estimated that the severity was lessened as compared with that experienced by subjects suddenly exposed to such a velocity. It was concluded that none of the patterns of stepwise increases in velocity resulted in accept- able levels of adaptation to the stress. In the next attempt, symptoms of motion sick- ness, with the probable exception of drowsiness, were prevented solely through control of the SRR velocity (ref. 9). The initial speed of rotation was 2 rpm, after which there were nine unit increases in velocity, with dwell times of 2 days at each level except terminal velocity (10 rpm) where the subjects remained for nearly 9 days. Four male subjects, 17 to 19 years of age, participated. All were healthy, and semicircular canal and otolith organ function was normal as revealed by the threshold caloric (ref. 10) and ocular counterrolling (ref. 11) test procedures. The diagnostic categorization used in estimating levels of severity of acute motion sickness is summarized in table 1 (ref. 12). After 3 days of familiarization with the test program, the subjects entered the SRR where they remained for about 32 days; the rotation period was nearly 25 days. They had a busy schedule except in the evening and at times made "experimenter-paced" head motions. The stress profile and the symptomatology are summarized in figure 1 (ref. 13). With the ex- ception of drowsiness, the subjects' symptoms were either trivial or explicable (due to power failure) in the perrotation period. Daily clinical evaluations by the onboard physician-experi- Category Pathognomonic, 16 points Major, 8 points Minor, 4 points Minimal, 2 points AQS, 1 point Vomiting or Nausea II, Nausea I Epigastric dis- Epigastric retching. HI. comfort. Pallor I awareness. Flushing/subjective Skin Pallor III Pallor II warmth, * II. Ill II I Ill II I Pain Ill II I Headache. Dizziness: eyes system. closed, ~Â» II; eyes open, III. Frank sickness (S) * 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 (MI) 1-2 points TABLE 1.âDiagnastic Categorization of Different Levels of Severity of Acute Motion Sickness l [AQS = Additional qualifying symptoms. Ill = severe or marked, II = moderate, I = slight] Levels of Severity Identified by Total Points Scored 1 From ref. 12.
PREVENTION OF MOTION SICKNESS IN THE SLOW ROTATION ROOM 111 menter, bolstered by routine hematological pro- cedures, urinalysis, and other laboratory tests, revealed no definite variations from control values. The results of the analysis of the excre- tion rates for catechol amines and 17-hydroxy- corticosteroids revealed no significant differences from baseline rates throughout the entire ex- perimental period. On cessation of rotation, ataxia was the most prominent and lasting com- plaint, and symptoms of motion sickness were either absent or trivial. ADAPTATION THROUGH CONTROL OF THE SUBJECT'S HEAD MOTIONS AND VELOCITY OF THE SRR The experiments described in the preceding section demonstrated that adaptation would occur in the absence of overt symptoms of motion sickness, but that long periods were required when reliance was placed only on "incidental" stressful head motions. It became apparent that the adaptation process should be speeded up by controlling the subject's head motions as well as the velocity of the SRR. Two experiments were conducted (ref. 14) in which the dwell time at each incremental in- crease in velocity of the SRR was determined by the capacity of the subject to make a given number of standardized head motions generating TABLE 2.-Susceptibility to Acute SRR Sick- ness (Dial Test) Rotation, Head Level of Subject rpm movements, symptoms' Experiment I: number TA 7.5 60 Mill SC 15.0 35 Mlll JE 20.0 70 Mill Experiment II: RO 20.0 300 MI CA 20.0 300 MIIA DA 20.0 75 Mill See table 1. 'MM 30 29 26 M e 20 -YR -DU -BR HO TIME IN DAYS MIA MIB MI â¢ ~ mi si',1 1 â¢â¢;<!. E'.c.r. J1J I I23456769 I0 tattfHMM 1*30 HOURS 12 I3 I4 13 I6 I? I6 I9 20 ?I 22 23 24 Â» Â» 27 Â» 29 50 3I 32 33 FIGURE 1. â The stress profile in the SRR and changes in level of motion sickness symptoms in four healthy subjects exposed to rotation over a period of nearly 25 days. (From ref. 13.)
112 THE ROLE OF THE VESTIBULAR ORGANS IN SPACE EXPLORATION Coriolis accelerations. The limiting factors were fatigue on the part of the subject and the periods required for sleep and other life-support activities. Three volunteer subjects partici- pated in each experiment. All six were college students, 18 to 23 years of age, and were selected mainly on the basis of clinical fitness and not on the basis of susceptibility to motion sickness. None had any significant loss in hearing, all had normal threshold caloric tests responses and ocular counterrolling indices, and scores made on postural equilibrium tests (refs. 15 and 16) were within the normal range. Their suscepti- bility to acute SRR sickness as revealed by the dial test is shown in table 2; note that the end- point, severe malaise (M III), was not reached by subjects RO and CA at the cutoff point; i.e., 300 head movements at 20 rpm. Experiment I The stress profile and summary of the findings in the first experiment are shown in figure 2. The subject's shoulders were restrained, and the movements consisted essentially of flexion of the head from the upright and return: about 70Â° forward, about 35Â° backward, and 45Â° left and right, always in the same order. The head movements were paced with a metronome set for 2 seconds at velocities of 1 to 6 rpm, 4 seconds at 7 to 9 rpm, and 6 seconds at 10 rpm. Standardized tasks were used to test for the effectiveness of transfer of adaptation to omni- directional motions at terminal velocity. Individual differences in susceptibility to motion sickness and in rate of adaptation to the stressful accelerations were revealed. TA was by far the most susceptible of the three subjects. He became drowsy at a very low level of stress, and this was followed by more severe symptoms at higher angular velocities; indeed, he was not able always to make the required number of head motions. To insure prevention of symptoms at 10 rpm in his case, a different program for the incremental increases in stress would be required. There were small but significant differences between the other two subjects. SC manifested very mild symptoms at 8 rpm while both SC and JE, for the first time. ME *M mvu I !iI. â¢ *TA rifIIMM ncwBM Â«f H-H, MCM* t*Ht TA M MI pwIicftIl 1KW4 UIUH â¢ IfftIA, In H-H 1 tatcnii Â«w mÂ»oÂ» iÂ«** 290 Â» 500 4 EwviMMw aMCM toil, TA *n pÂ«' TA SC JE n ^-'u r MIA MOB MI |600 2000 2400 0400 0600 '600 2000 ?400 0400 0800 TIME OF DAY Fl(;URE 2. â The stress profile in the SRR and manifestations of motion sickness in three healthy subjects exposed to rotation for over 2 days. (From ref. 14.)
PREVENTION OF MOTION SICKNESS IN THE SLOW ROTATION ROOM 113 manifested symptoms when required to carry out the standardized tasks at terminal velocity, indi- cating that the adaptation acquired making the standardized (limited) head motions did not afford full protection (incomplete transfer) during activities involving omnidirectional head rotations of maximal excursion. Experiment II The stress profile of the second experiment, along with a summary of the findings, is shown in figure 3. The duration of rotation in the SRR was a little over 2 days, during which time the subjects made 1000 head movements at each one- unit increase in velocity, except at 10.0 rpm when they made 500 and then participated in gener- alized activities. These sessions occupied about 4 to 5 hours of each day, and there were no re- strictions on the subject's moving about at other times. In this experiment the subjects were secured by means of a lap belt, and the move- ments involved not only flexion of head but also movement of the trunk at the waist. The back of the chair limited backward motion to about 40Â°, but the movements sideways were about 70Â° and those forward, 90Â°. The findings revealed that one subject, DA, did not manifest any overt symptoms of motion sickness either perrotation or during the post- rotation period, while in the other two the symp- toms were either trivial (CA) or mild (RO). It is also noteworthy that all of the subjects were ataxic on attempting to walk after cessation of rotation. DISCUSSION The cardinal findings in these experiments have important theoretical and practical implica- tions which are discussed below. Theoretical Implications The fact that adaptation to strong Coriolis accelerations can occur in the absence of overt symptoms of motion sickness is proof that the *M u,i,,.-., ISItfii IQsmn M 1000 J Bfcoin â¢Â» <eiu> ol SCO -ad mÂ»Â»i-.n 1 n 1 PÂ»iM ci npeiiwm dncM MiI rÂ« '"Â» .y --CA j , i 22 DA "Â° fj 1 M i, KB "0 1 1 II 14 It 10 P MB ?, 1Â° *Mm 1000 oe woo p H MHA 1000 2 MHB MI mo 0 1 . . , , , ... . .,./.;â¢,,. ,' ,7/1 â¢â¢.â¢â¢"â¢" V ~ ~.~.~ ."â¢. ~".~ . V ""././, .,.,.," .â¢ . , â¢, TIME Of DAY FIGURE 3. â The stress profile in the SRR and manifestations of motion sickness in three healthy subjects exposed to rotation for about 2 days. The large number of head motions accounted for the rapid adaptation. (From ref. 14.)
114 THE ROLE OF THE VESTIBULAR ORGANS IN SPACE EXPLORATION adaptive processes need not involve the neural processes and events immediately responsible for motion-sickness symptoms. In other words, by preventing symptoms it was demonstrated that what is sometimes referred to as "habitua- tion of symptoms" did not occur and raised the question whether it ever occurs. Groen (ref. 17) has discussed both the nature and possible sites of the adaptation processes. There was evidence of transfer of adaptation acquired at a given angular velocity of the SRR to a higher velocity; also, adaptation acquired through limited head excursions in two planes of arc transferred to omnidirectional head motions of unlimited excursion, provided a sufficient number of discrete motions had been made. There was some evidence in our studies that overadaptation at 10 rpm minimized or abolished the susceptibility to symptoms on cessation of rotation, suggesting a "general suppression" effect with the exception that it was direction specific; adaptation in a clockwise direction in- creased susceptibility to symptoms during ex- posure to a counterclockwise rotation. On ces- sation of rotation, after long exposure at 10 rpm, ataxia was prominent even when symptoms of motion sickness were absent, implicating non- vestibular and somatosensory systems. Another implication, based on findings in present and previous experiments in the SRR (refs. 1 to 4), is that when symptoms do occur, they represent a "failure" in homeostatic proc- esses. This failure is due to exposure to Coriolis accelerations, the stressor, which exceed the capacity of the organism to adapt. In other words, the "functional vestibular reserve" rep- resenting the adaptive capacity has been ex- ceeded, and symptoms of failure appear. The strength of the stressor per se is not important, but its strength vis-a-vis the reserve is all im- portant. Some of the characteristics of natural or innate reserve are shown by interindividual differences in susceptibility to motion sickness in persons with little or no previous exposure in unusual force environments. Going beyond the limits of the functional reserve or a failure of homeostasis presumably allows, through the processes of facilitation and inhibition, irradia- tion of vestibular activity to areas not stimulated under natural conditions. The initial responses implicate the visceral nervous system, but these effects are followed by second- and third-order effects, some of which are in the nature of "com- plications" (refs. 18 to 20). Although it is well known that a person may be more susceptible to motion sickness in one force environment than another, there is no evidence that vestibular mechanisms underlying the symptomatology are not generally applicable. Practical Implications The findings in these experiments point the way toward the prevention of motion sickness by "natural" means if it is decided to generate artificial gravity by causing a spacecraft to rotate. Adaptation could be effected without evoking significant symptoms of motion sickness through control over the angular velocity of the spacecraft and through the astronauts' control over head rotations out of the plane of the spacecraft's rotation. Additional observations must be made to determine the best profiles, taking into account the number of stepwise increases to terminal velocity and individual adaptability, not only under terrestrial conditions but also at given subgravity levels. With regard to the former, it may be pointed out that all persons have some vestibular reserve in a rotating environment under terrestrial condi- tions, but that, for some persons, this reserve is nil in weightlessness even in the absence of rotation and even may be exceeded; i.e., symp- toms may be evoked with head motions (ref. 21). Obviously, the incremental increases would be differently patterned in the case of astronauts selected for low susceptibility compared with an unselected group of astronauts. It is also essential to keep in mind that adaptation does not occur with head fixed, such as would be the case while astronauts were sleeping or while engaged in tasks not requiring head motions out of the plane of rotation of the spacecraft. For a given pattern of changes in angular velocity and the accompanying changes in g- loading which would be a function of the effective radius, e.g., position of the astronaut, the remain- ing aspects in control of the vestibular stimulation would rest almost entirely with the individual. The greater the number of stressful accelerations.
PREVENTION OF MOTION SICKNESS IN THE SLOW ROTATION ROOM 115 the more rapid the adaptation, although addi- tional guidelines are important. Overt symp- toms of motion sickness should be avoided, although it is reasonable to believe that levels of stress just within the tolerance limits are the most effective. Some experience is needed to avoid summation or cumulation effects. Very mild acute symptoms quickly disappear with head fixation. Details concerning the most efficient way to effect adaptation need to be worked out as well as the best means of avoiding symptoms while a susceptible astronaut is carrying out essential tasks. Return to a stationary environment, or quick transfer back and forth between a rotating and stationary environment presents little or no problem from the standpoint of motion sickness but may with regard to ataxia which is, in very large degree, a separate problem (refs. 22 and 23). REFERENCES 1. GRAYBIEL, A.; CLARK, B.; AND ZARRIELLO, J. J.: Observa- tions on Human Subjects Living in a "Slow Rotation Room" for Periods of Two Days. Arch. Neurol., vol. 3, 1960, pp. 55-73. 2. CLARK, B.; AND GRAYBIEL, A.: Human Performance During Adaptation to Stress in the Pensacola Slow Rotation Room. Aerospace Med., vol. 32, 1961, pp. 93-106. 3. GRAYBIEL, A.; KENNEDY, R. S.; KNOBLOCK, E. C.; GUEDRY, F. E., JR.; MERTZ, W.; MCLEOD, M. E.; COLE- HOUR, J. K.; MILLER, E. F., II; AND FREGLY, A. R.: The Effects of Exposure to a Rotating Environment (lOrpm) on Four Aviators for a Period of Twelve Days. Aero- space Med., vol. 36, 1965, pp. 733-754. 4. GUEDRY, F. E., JR.: Habitation to Complex Vestibular Stimulation in Man: Transfer and Retention of Effects From Twelve Days of Rotation at 10 rpm. Percept. Mot. Skills, vol. 21, 1965, pp. 459-481. 5. STONE, R. W., JR.; AND LETKO, W.: Some Observations on the Stimulation of the Vestibular System of Man in a Rotating Environment. The Role of the Vestibular Organs in the Exploration of Space, NASA SP-77, 1965, pp. 279-292. 6. NEWSOM, B. D.; BRADY, J. F.; AND GOBLE, G. J.: Equilib- brium and Walking Changes Observed at 5, 7i, 10. and 12 rpm in the Revolving Space Station Simulator. Aerospace Med., vol. 36, 1965, pp. 322-326. 7. LETKO, W.; AND STONE, R. W., JR.: The Effects of the Plane of Vestibular Stimulation on Task Performance and Involuntary Eye Motion. Third Symposium on the Role of the Vestibular Organs in Space Explora- tion, NASA SP-152, 1968, pp. 49-55. 8. BERGSTEDT, J.: Stepwise Adaptation to a Velocity of 10 rpm in the Pensacola Slow Rotation Room. The Role of the Vestibular Organs in the Exploration of Space, NASA SP-77, 1965, pp. 339-344. 9. GRAYBIEL, A.; DEANE, F. R.; AND COLEHOUR, J. K.: Pre- vention of Overt Motion Sickness by Incremental Ex- posure to Otherwise Highly Stressful Coriolis Accelera- tions. Aerospace Med., vol. 40, 1969, pp. 142-148. 10. McLEOD, M. E.; AND MEEK. J. C.: A Threshold Caloric Test: Results in Normal Subjects. NSAM-834. NASA Order R-47. Naval School of Aviation Medi- cine, Pensacola, Fla., 1962. 11. MILLER, E. F., II: Counterrolling of the Human Eyes Produced by Head Tilt With Respect to Gravity. Acta Oto-LarynRol., vol. 54, 1962. pp. 479-501. 12. GRAYBIEL, A.; WOOD. C. D.: MILLER. E. F., II; AND CRAMER, D. B.: Diagnostic Criteria for Grading the Severity of Acute Motion Sickness. Aerospace Med., vol. 39,1968, pp. 453-455. 13. GRAYBIEL, A.: Structural Elements in the Concept of Motion Sickness. Aerospace Med., vol. 40, 1969, pp. 351-367. 14. GRAYBIEL, A.; AND WOOD, C. D.: Rapid Vestibular Adaptation in a Rotating Environment by Means of Controlled Head Movements. Aerospace Med., vol. 40. 1969, pp. 638-643. 15. GRAYBIEL. A.; AND FREGLY, A. R.: A New Quantitative Ataxia Test Battery. Acta Oto-Laryngol., vol. 61, 1966, pp. 292-312. 16. FREGLY, A. R.; AND GRAYBIEL. A.: An Ataxia Test Battery Not Requiring Rails. Aerospace Med., vol. 39,1968, pp. 277-282. 17. GROEN, J. J.: Adaptation. Pract. Oto-Rhino-Laryngol., vol. 19.1957, pp. 524-530. 18. McNALLY, W. J.; AND STUART, E. A.: Physiology of the Labyrinth Reviewed in Relation to Seasickness and Other Forms of Motion Sickness. War Med., vol. 2,1942, pp. 683-771. 19. TYLER. D. B.: AND BARD. P.: Motion Sickness. Physiol. Rev., vol. 29,1949, pp. 311-369. 20. 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. 21. MILLER. E. F., II; GRAYBIEL, A.; KELLOGG, R. S.; AND O'DONNELL, R. D.: Motion Sickness Susceptibility Under Weightless and Hypergravity Conditions Generated by Parabolic Flight. Aerospace Med., vol. 40.1969, pp. 862-868. 22. GRAYBIEL, A.: Vestibular Problems in Prolonged Manned Space Flight. Presented at the Vestibular Symposium Sponsored by the Barany Society. Upp- sala, Sweden, May 29-30,1968. 23. GRAYBIEL, A.: Vestibular Mechanisms in Human Behavior. Ann. Otol.. vol. 77, 1968. pp. 772-786.
116 THE ROLE OF THE VESTIBULAR ORGANS IN SPACE EXPLORATION DISCUSSION Lansberjc: Do you think the effect will linger once the man has become habituated and he has left the rotating room after a month or after 6 weeks? Graybiel: No, I do not. He loses this quite rapidly. Laiisberg: The habituation has to be rebuilt? Graybiel: Yes. He remains habituated for a little while, but even within 48 hours it appears as though it is decreasing. However, the subject does seem to retain a little extra protec- tion as compared to what was present before. We have not really studied this systematically. Bald.es: Have you tried any experiments on hypnosis in your rotating room? Graybiel: We had one young medical officer who practiced autohypnosis. He was able to prevent motion sickness while making head movements at 20 rpm during the provocative dial test. This required considerable effort on his part. Prior to the exposure, 1 found him lying on a couch. I asked him if he was unwell. He said, "No," and that he was "just concen- trating and getting set." We have precipitated one mild attack of petit mal. On two occasions we have precipitated a severe circulatory collapse in a highly susceptible person. Symptoms due to a fall in blood pressure are extremely rare in our experience. Newsom: I am glad to see the confusion between our two studies has finally been cleared up. As you recall, we re- ported at the first symposium in 1965 (Newsom, Bernard D.; and Brady, James F.: "Observations on Subjects Exposed to Prolonged Rotation in a Space Station Simulator," NASA SP-77. 1965, pp. 279-292) that there were no symptoms after stepwise adaptation. Even more surprising was that we had no postrotation effects. There were no postrotation effects providing the man kept his eyes open. Did you do any blind rail walking or blind balancing? Graybiel: We have performed a number of experiments indicating that symptoms of motion sickness and manifesta- tions of ataxia in the rotating room, though commonly asso- ciated, can be "uncoupled." This was clearly demonstrated in an experiment involving the use of air-bearing supports and articulated Fiberglas molds which permitted the subjects to carry out activities, including walking, when in the Earth- horizontal position. While rotating for 2 days in the "hori- zontal mode," they experienced symptoms of motion sickness which disappeared through the mechanisms of adaptation. Then they were taken out of the molds and exposed for an additional 2 days when upright. In this vertical mode they experienced ataxia but not motion sickness. When the first 2 days were spent upright, they experienced both ataxia and motion sickness which gradually disappeared. The last 2 days were spent in the molds without complaints, and they remained in the molds for a day and a half following cessation of rotation. Soon after rotation ceased, mild symptoms of motion sickness appeared on making head movements. On getting out of the molds they experienced ataxia as the result of adaptation to the rotating environment acquired 34 days previously; obviously different mechanisms were involved.