* DOTIFAA/AM-86/9 EFFECTS OF SLEEP LOSS ON

Office of Aviation Medicine VESTIBULAR RESPONSE DURING

Washington, D.C. 20591 SIMPLE AND COMPLEX

VESTIBULAR STIMULATION

William E. Collins, Ph. D.

Civil Aeromedical Institute

Federal Aviation Administration

Oklahoma City, OK 73125

(V~) July 1986

* Flonal Report

This document is available to the public 

through the National Technical Information

Service, Springfield, Virginia 22161

~DTIC

F!-ECTE

LLJ US. Department of Transportation C tj18

Federal Aviation Administration

a 

iza

-.. C=*- :..........~. -- ~.*
DOT/FAA/AM-86/9 EFFECTS OF SLEEP LOSS ON VESTIBULAR 1~ RESPONSE DURING SIMPLE AND COMPLEX

Office of Aviation Medicine VESTIBULAR STIMULATION

Washington, D.C. 20591

William E. Collins, Ph.D.

Civil Aeromedical Institute

Federal Aviation Administration% 

Oklahoma City, OK 73125

July 1986 

2'-)T 1986

Final Report

This document is available to the public

through the National Technical Information

Service, Springfield, Virginia 22161

U.S. Department of Transportation

Federal Aviation Administration

~~~~~~ .. .% . . .* .. . . . * * * - . N . *
Technical keport Documentation Page 

1. Report No. 2 Governient Accesson No. 3. Rec,pient s Catalog No

FAA-AM-86- 9

4. Title and Subtitle 5. Report Date

EFFECTS OF SLEEP LOSS ON VESTIBULAR RESPONSE July 1986

DURING SIMPLE AND CGIMPLEX VESTIBULAR STIMULATION 6. Perform..ing Orga .. o..o Code 

____, _ . ....... 8.___ Performing Organ .ton Report No, 

7. Author's)

William E. Collins, Ph.D. 

9. Performing Organization Name and Address 10 Work Unit No (TRAIS)

- FAA Civil Aeromedical Institute

P. 0. Box 25082 11 Contract or Grant No.

Oklahoma City, Oklahoma 73125

13. Type of Report and Period Coered

12. Sponsoring Agency Nome and Address

Office of Aviation Medicine

,.. Federal Aviation Administration

800 Independence Avenue, S.W. 14. Sponsoring Agency Code

Washington, D.C. 20591 -:"_ __'_-.'_ _

15. Supplementary Notes

This work was performed under tasks AM-D-75-PSY-54 and AM-D-86-PSY-94.

.-. 

16 Abstract>Few data are available concerning the effects of sleep loss on vestibular

*-" responses -although those responses are significant products of motion in aviation 

I environments. This study assessed periodically throughout6.period of/ approximately.. 

55 hrs. of sleep loss the ocular nystagmus and motion experiences of'men exposed to

* both simple (angular acceleration) and complex (Coriolis) vestibular stimulation.

"N. The effects on those reponses of an alerting drug administered after 54 hr of sleep

5. I loss were also examined. Control and sleep-deprived groups each comprised 10 young

, men. Angular accelerations and Coriolis stimulation (30-deg head movements during

* CW rotation) were accomplished in an enclosed Stille-Werner rotating device.

Nystagmus and motion experiences (turning, "diving," and "climbing") were recorded

throughout each session. Tests were given at 0900 and 1300 on each of 3 successi

days. Subjects ingested 10-mg of d-amphetamine at 1200 on Day 3. During simple

stimulation, the sleep-deprived group showed regular declines across sessions in

slow phase and duration measures of nystagmus but fast phase ocular frequency and

* measures of experienced turning resisted declines until the final predrug session;

response latencies increased with sleep loss. Declines during rotation for ocular

output and measures of perceived displacement during rightward head tilts 

("climbing" sensation) were obtained for the sleep deprived, but both nystagmus and

sensations were unaffected by return (leftward) movements of the head ("diving"

sensation). d-Amphetamine had no consistent effect on either the ocular or

i subjective responses of control subjects, but significantly increased nystagmus and 

elevated (but not significantly) measures of turning experiences for the sleep

- deprived. Statement

17 Key Words 18. Distribution Statement

*" Sleep Deprivation Drug Fffects Document is available to the public through 

-Vest ihular the National Technical Information Service, 

Nvstagmus Springfield, Virginia 22161

Coriolis nystagmus

,-. Cortolls sunsat ions m 1. S~curty Clansf. (of , rport 20. Security Clossif. (of this page. 21. No ofPage T22Pce

UncassfiI I..------- Unclassified -.---- 7 . 

Form DOT F 1700.7 8-:2 Reproduction of completed page utnhori red 
EFFECTS OF SLEEP LOSS ON VESTIBULAR RESPONSES DURING

SIMPLE AND COMPLEX VESTIBULAR STIMULATION

The known effects of sleep loss c. vestibular responses are meager. Wolfe and 

Brown 12 gave each of 16 subjects two trials (one 8 deg/sec 2 acceleration and

one 24 deg/sec 2 deceleration) before and after 24 hrs of sleep loss. Of four 

measures of nystagmus (slow-phase, frequency, duration, threshold) only the

frequency counts for the 24 deg/sec 2 stimulus differed significantly from pre- 

to posttest; frequency was higher during the posttest, but the absence of a

control group makes interpretation difficult. Dowd, Moore, and Cramer)

reported no difference in the occurrence of motion sickness between rested and

sleep deprived (24-hr) military pilots (N=131) during laboratory Coriolis

stimulation, but differences in decay rates of vertical nystagmus and in

"sensitivity" (a product of maximum eye velocity and decay rate of vertical

components of nystagmus) were obtained. The design of the study, however, was

such that clear attribution of the effects to sleep loss was not possible and 

results were presented from only one direction of head movement (that yielding

sensation of a 'rolling climb"). Dowd4 tested an additional group of 38

pilots and apparently included 105 subjects from the study noted above (the 26

pilots who had shown motion sickness symptoms were excluded) yielding a total

of 143 experienced pilots divided into three groups (rest/rest, rest/sleep 

deprived, sleep deprived/rest); he reported a significant increase in the

sensitivity measure and a significant decrease in the decay rate of vertical 

nystagmus (from a single head movement) following 24 hrs of sleep loss. He

interpreted that increase as a weakening of vestibular suppression acquired 

through flying activities. 

While nystagmus measures are important manifestations of vestibular function,

the sensations of motion experienced during simple angular accelerations and

Coriolis-type (complex) stimulation are especially significant in aviation

environments. The present study was designed to assess the effects of sleep

loss on a number of vestibular and vestibular-related responses including

nystagmus and sensations over a longer period of sleep deprivation

(approximately 55 hr) than previously investigated.

METHOD

Subjects. A control group and a group of sleep-deprived subjects each

comprised 10 men, paid volunteers, 21-28 years old (mean age 23.3 years). All

subjects remained under constant monitoring in the laboratory for the three

experimental days. Half the subjects were allowed to sleep; the other half

were kept awake and active. Subjects were asked to abstain from alcoholic

drinks for 48 hours prior to the study, to arrange to have 8 or more hours of

sleep on the night prior to the first experimental day, and to rise at 0700.-.. 

Subjects were not allowed to consume caffeine drinks or to smoke throughout 

the study. 

The assistance of Gregory N. Constant, Patricia Gant, Linda Foreman, Cissy

Lennon, J. M. Lentz, and RuthAnn Parvin in the conduct of this study and of 

Deborah K. Taylor for aid in data analysis is gratefully acknowledged. 

p....

.. . 
Procedure. Angular accelerations and Coriolis stimulation were accomplished

head was fixed in a head-holder; a bite-block helped to position the

horizontal semicircular canals approximately in the plane of rotation.' The

room was in total darkness and the head-holder was adjusted to permit uniform

head tilts of 30 deg to the right and a return movement (30 deg to the left)

to an erect head position. Subjects were instructed to keep their eyes open

during trials and were periodically reminded to do so prior to each angular 

acceleration and each instruction to move their heads.

Each subject was accelerated clockwise at an angular rate of 5 deg/sec 2 for 18

sec to a constant velocity of 90 deg/sec; during this time he signaled his

turning sensations. The signals were depressions of a microswitch to indicate 

when the subject experienced the start, successive 90 deg angles of turning,

and the end of his turning sensations.

After approximately 3 min of constant rotation and following the cessation of

the turning sensations, the subject was instructed to tilt his head to the

right and, later, to return his head to an erect position. Each head tilt

required about 1 sec and a rest period of at least 1 min followed the end of

the response to each tilt and each return movement. The subject used the

microswitch to signal the start and end of each "climbing" (head tilt) or

"diving" (head return) sensation and then provided a verbal estimate of the 

number of deg of "climb" or "dive" he experienced. The chair was decelerated 

to a stop at 5 deg/sec2 with the subject, head upright, signaling his turning

experiences.

One day prior to the experimental sessions, subjects were given instructions'-,

and then participated in a set of familiarization trials to acquaint them with

forms of stimulation produced by a laboratory rotator and to give them

experience in signalling and rating their experiences of motion. This was 

followed by a formal practice session during which performance on each test 

was recorded.

Experimental tests were given at 0900 and 1300 on each of the 3 successive

experimental days. Each subject ingested a 10-mg capsule of d-amphetamine

sulphate at 1200 on Day 3. Scrn

Scoring 

Turning Experiences. The turning motions experienced by both groups of

subjects were examined in three ways. Calculations were made of (i) the

latency of the response in sec (the time from the start of physical turning to

the first signal of experienced turning), (ii) the duration of perceived

turning in sec (the time from the first signal of experienced turning to the

signal indicating the end of experienced turning), and (iii) the amount of

experienced turning in deg (90 deg times the total number of turning signals

minus 2--the two omitted signals being the indications of the start of turning

and the end of turning).

Coriolis Sensations. Two measures of Coriolis sensations were obtained. The

first was duration in sec of the climbing or diving experience resulting from

head movements during rotation. Subjects depressed a microswitch when the

sensation began and when it ended. The other measure was magnitude in deg of

perceived climb or dive. Subjects estimated the amount of perceived motion in
the vertical plane; i.e., they estimated their peak apparent displacement in

deg above ("climb") or below ("dive") an earth-horizontal plane.

Vestibular Nystagmus. Three measures of the horizontal components of 

nystagmus occasioned by angular accelerations and decelerations were obtained 

from the tracings, viz, slow-phase displacement, number of fast phases, and

duration of response. The same measures were obtained for vertical components of nystagmus occasioned by head movements during rotation. Conversion of..-.-

slow-phase measures into deg of eye movement was accomplished by means of

calibrations obtained with two sets each of two small alternately flashing

lights, subtending a visual angle of 15 deg in the horizontal plane in one 

case, and 15 deg in the vertical plane in the other case.

L RESULTS

Statistical Analyses. In all cases, data for a given condition/measure (e.g.,

acceleration/nystagmus duration) were analyzed first by multivariate analysis 

(MANOVA) techniques for repeated measures and then by t tests in making paired

comparisons. Separate sets of analyses (tables 1 and 2) were accomplished for

(i) the first session (Day 1, 0900), the fifth session (Day 3, 0900), and the

postdrug session (Day 3, 1300) to isolate the effects of conditions (i.e.,

sleep loss and drug), and (ii) for the first five sessions (Day 1, 0900

through Day 3, 0900) to clarify successive effects. The second set of 

analyses (see tables 3, 4, and 5) is occasionally noted in the text as an aid

to interpreting findings from the main analyses.

Rotation-Induced Nystagmus. For the control group, nystagmus measures stayed

relatively constant or showed a shallow decline across sessions (see figure

1). Results of the MANOVAs (table 1) and the paired comparison tests (table

2) indicated that there was no significant change in nystagmus output for the

fifth vs. the first session to either acceleration or deceleration stimuli 

(in fact, there were no significant differences between any pairings of the 

first five sesions for any nystagmic measure; see tables 3 and 4). Ingestion

of d-amphetamine by control subjects had minimal effect, viz. for

decelerations only, it increased the duration measure for the postdrug session 

significantly above that of session 5 and increased the fast phase frequency

score for the postdrug session significantly above that of the first session

(p < .05 in both cases).

For sleep-deprived subjects, all measures of nystagmus during session 5 were

below (p < .01) those of the first session for both acceleration and 

deceleration. Thus, sleep deprivation produced an overall decline in output

of nystagmus (see table 2). The ingestion of d-amphetamine uniformly

increased ocular output; that increase was significant in comparisons of the

postdrug session vs. session 5 for all measures of nystagmus during

acceleration stimuli, and for the fast phase frequency of nystagmus during

decelerations. These significant increases elevated the postdrug scores

sufficiently that they did not differ from the scores obtained in the first

session. Where the postdrug increases were not significantly above session 5

(i.e., for duration and slow phase measures during deceleration), the output 

of nystagmus remained significantly (p < .01) below the first session

measures.
ACCELERATION DECELERATION 

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DURATION OF VESTIBULAR NYSTAGMUS PRODUCED BY ANGULAR ACCELERATIONS AND"""'"

DECELERATIONS (5 DEG/SEC2 ) ACROSS 6 SESSIONS FOR CONTROL AND SLEEP DEPRIVED

SUBJECTS. THE 0 SCORES REPRESENT THE BASE LEVELS (FIRST SESSION) OF OCULAR

*OUTPUT; SCORES FOR SUCCESSIVE SESSIONS WERE CONVERTED TO PERCENTAGES OF" 

INCREASE OR DECREASE FROM THE BASE LEVELS. THE DRUG (10 MG D-AMPHETAMINE 

SULPHATE) WAS ADMINISTERED AT 1200 ON DAY 3. 

LPr

* It 2_ 

Coriolis Nystagmus. The control group maintained its output of nystagnus for 

several Coriolis measures (from head movements) or showed only a slighit 

tendency for responses to decline across sessions (see figure 2). The control 

group showed no significant changes in output of nystagmus for sessions 1 vs 5 

'" to either tilts or return movements of the head (see table 2). Ingestion of 

d-amphetamine had minimal effects; it resulted in a significant (p < .05) drop-.----%

(compared with session 1) in slow phase output during head tilts, and it-[.,

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produced an increase in fast phase output during return head movements that

made the postdrug score for frequency of nystagmus significantly greater than

those of both sessions 1 and 5 (P < .05 in both cases).

40 HEAD TILT (Climb) HEAD RETURN (Dive)

SSLEEP DEPRIVED

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TEST SESSIONS

FIGURE 2. CHANGES IN FAST PHASE FREQUENCY, SLOW PHASE DISPLACEMENT, AND

DURATION OF CORIOLIS VESTIBULAR NYSTAGMUS PRODUCED BY ACTIVE HEAD MOVEMENTS (A

% TILT 30 DEG TO THE RIGHT; A TILT 30 DEG TO THE LEFT TO RETURN THE HEAD TO

UPRIGHT) DURING CW ROTATION AT 90 DEG/SEC. DESIGNATIONS IN THE GRAPHS ARE THE

SAME AS IN FIGURE 1.

For the sleep-deprived group, nystagmus scores from head tilts dropped sharply

and regularly across predrug sessions; scores for return-to-upright movements

of the head showed less consistent and weaker tendencies to decline.

Significant reductions in nystagmic output for sessions 1 vs. 5 occurred for

all measures (p < .01) during head tilts, and only for the slow phase measure

* (p < .05) during head returns. Although the drug sufficiently elevated ocular

10 

% N
output in all cases of significantly reduced responses so that the postdrug

session measures showed no significant differences from session 1, only the

duration and fast phase frequency measures for head tilts rose significantly" 

(p < .01) above those for session 5. 

Turning Experiences. The duration of turning experiences occasioned by

angular accelerations and decelerations showed declining trends for both

groups of subjects (see figure 3). However, only the deceleration stimulus

for the control group yielded a significant (p < .05) decline for session 1 vs

5. (Duration scores for sessions 2, 3, and 4 all declined significantly from 

session 1 for acceleration stimuli for the control group, but the duration 

score was considerably elevated in session 5. This elevated score might, for

this measure, lead to an underestimation of the effect of sleep loss.) The 

ingestion of d-amphetamine produced no consistent or significant effect,

slightly elevating duration scores for the sleep-deprived, and slightly

lowering them for the control group.

The amount of turning experienced during accelerations and decelerations

showed almost no change across sessions for control subjects. There was a

drop (that was short of being statistically different from session 1) only

o ACCELERATION DECELERATION I-- .. 40 r 4 0 r < • '- C O N T R O L F

D) 20-~~ SLEFP CEPRIVE:2 2D.

0

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TEST SESSIONS

FIGURE 3. CHANGES IN THE DURATION AND AMOUNT OF TURNING EXPERIE CED AS A

RESULT OF ANGULAR ACCELERATIONS AND DECELERATIONS (5 DEG/SEC ) ACROSS 6

SESSIONS FOR CONTROL AND SLEEP DEPRIVED SUBJECTS. DESIGNATIONS IN THE GRAPHS

ARE THE SAME AS IN FIGURE 1.

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44040V° ACCELERATION 440 DECELERATION

420 L l- CONTROL 420

(f) 400 DEPRIED 400"

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0900 ,500900 1300 0900 300 0900 1300 0900 1300 0900 '300

TEST SESSIONS

FIGURE 4. CHANGE IN THE LATENCY (THE TIME BETWEEN STIMULUS ONSET AND THE

FIRST SIGNAL) OF THE TURNING RESPONSE TO ANGULAR ACCELERATIONS AND

DECELERATIONS FOR CONTROL AND SLEEP DEPRIVED SUBJECTS. DESIGNATIONS IN THE

GRAPHS ARE THE SAME AS IN FIGURE I. 

during the fifth session for the sleep-deprived group; however, because scores

increased somewhat across the first four sessions, the total displacement

scores for the fifth session were significantly (p < .05) below those of each

of the two preceding sessions for the sleep-deprived subjects. The analeptic

drug elevated scores above those of session 5 (to both acceleration and

deceleration) for the sleep-deprived subjects, but no statistically

significant drug-induced changes were obtained. (The postdrug,

acceleration-induced, displacement score for the sleep-deprived group

increased considerably, but the increase was due largely to an inordinately

high signalling rate from one subject. That response represented an increase 

of approximately 250% over any previous response from that man, whose

signalling rate was initially high. His deceleration-induced displacement

score was also high, but his nystagmic output was not remarkably affected.

Perhaps he was unusually sensitive to the d-amphetamine.)

The latency of signalling turning experiences declined regularly, but not

significantly, for control subjects. For sleep-deprived subjects, latency

scores tended to increase across sessions and were significantly longer for

session 5 vs session 1 (p < .01 for both acceleration and deceleration).

d-Amphetamine reduced signal latencies for the sleep-deprived and had no reliable effect on the performance of control subjects.

12
Coriolis Experiences. For both groups, the duration of the Coriolis

"climbing" (pitch up) and "diving" (pitch down) experiences showed shallow

declining trends that did not reach statistical significance. The ingestion

of d-amphetamine produced no noticeable effect on this measure. (See figure

4.)

For both groups, the amount of perceived displacement during head tilts

("climb") showed a relatively regular decline across sessions. The decline 

from session 1 to 5 was significant for both groups (p < .05). Administration 

of d-amphetamine produced no discernable effect (scores dropped further) and

so the postdrug displacement scores were also significantly below those of

session 1 (p < .05 for the control group; p < .01 for the sleep-deprived).

For return movements of the head ("diving" sensations), displacement scores

tended to increase during the first four sessions and then declined slightly

during session 5. Differences between sessions 1 and 5 were not significant

(and were numerically higher for session 5) and the drug produced no reliable 

effect on these displacement measures (control group scores rose; the scores

for the sleep-deprived declined).

LLJ >(/.-5.- HEAD TILT (Climb) HEAD RETURN (Dive) 

W' 0 -- -C,ONTROL O~ 

O u 20i ,----. SLEEP DEPR ,ED 20-5 

Sz

z _ 

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DAY I -~DAY 2 -' DAY 3 - ~ ,-Y - DAY 2- -DAY 3 

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C1 TEST SESSIONS

FIGURE 5. CHANGES IN THE DURATION AND AMOUNT OF DISPLACEMENT EXPERIENCED AS A

RESULT OF ACTIVE TILT (RIGHTWARD) AND RETURN (LEFTWARD TO UPRIGHT) HEAD

MOVEMENTS DURING CW ROTATION AT 90 DEG/SEC. DESIGNATIONS IN THE GRAPHS ARE

THE SAME AS IN FIGURE 1. 

%--- . . .. 4 . .. .. . 

l..IA ,- ,o 
DISCUSSION 

These results show that the ordinary effects of sleep loss on vestibular

responses to a moderate angular stimulus are: (i) negligible effects on

quantified experiences of turning, (ii) a general decline in slow phase and

duration measures of nystagmus, and (iii) no reductive effect on fast phase 

nystagamus until sometime between 30-50 hrs (i.e., subsequent to the Day 2

session at 1300) of sleep deprivation. These findings agree with the

nystagmus results obtained by Wolfe and Brown 12 to their "moderate" stimulus 

(8 deg/sec 2 ) and extend from 24 to 50 hrs the period over which the nystagmic response during sleep deprivation is described.

Although Wolfe and Brown 1 2 had their subjects signal the onset and conclusion

of their rotary responses, they reported only latency data and found no preto-posttest change (to either their 8 deg/sec 2 or 24 deg/sec 2 stimuli) for a 

24-hr period of sleep deprivation. Our results show a small but steady

reduction in latency (i.e., quicker responses) for control subjects and

increasing latencies for the sleep deprived. Two factors in our latency data

for the sleep deprived S.. are worth noting: (i) with latencies during the first 

two sessions averaging about 5.5 sec, the marked increase during accelerations

on the mornings of Days 2 and 3 are largely attributable to two subjects (Day

2) whose latencies exceeded 13 sec and to 3 subjects (Day 3) whose latencies

exceeded 15.5 sec. This gradual increase probably reflects the individual

variability in response to sleep deprivation since latency scores do not show

a rise for all sleep deprived subjects until the afternoon of Day 2. (ii)

Latencies for the sleep deprived to accelerations showed markedly more

session-to-session variability and proportionately greater increases than did 

latencies to decelerations. This difference may be attributable to arousal

(or to potentiating effects in sleep deprivation) induced by the positive 

acceleration followed by the Coriolis stimulation shortly before the..-

decelerations were introduced. There was no indication of any consistent 

differences for accelerations vs. decelerations in responses from the control 

subjects.

The above rationale for explaining variations in our lat?5cy data may also

account for the lack of change noted by Wolfe and Brown in their latencies

after 24 hrs of sleep deprivation, viz. their stronger stimuli may have been

sufficiently more arousing as to prevent a noticeable lengthening of response

time for the proportionately few subjects (as suggested by our data) who would

have been negatively affected by 24 hrs of sleep deprivation.

Coriolis stimulation caused by rightward head tilts during CW rotation

produced a pattern of nystagmus across sessions that was similar to, but more

exaggerated than, the results obtained from angular accelerations. That is,

all three measures of nystagmus declined over sessions for sleep deprived

subjects while the control group showed a declining tendency for slow phase

and duration measures and a tendency for increased fast phase output. Moving

the head back to an erect position (i.e., a leftward movement during CW

rotation) produced nystagmus that showed no clear tendency to decline for 

control subjects and that seemed mostly resistant to reduction for the sleep

deprived; for the latter group (i) only slow phase measures were consistently

below the first session's output (and most of that decline occurred from the

14

,. .. .... ..- .. . - . 4. ... *.. . . . . . : - . . . - . . . -. . .. . . . . - . .. . - 
morning to the afternoon session on the first day) and (ii) the fast phase

output showed no drop until the morning of the third day (i.e., after sometime 

between 30-50 hrs of sleep deprivation).

These Coriolis findings are not directly comparable to Dowds4 results since

Dowd (i) used Air Force pilots who were regarded as having been habituated to

vestibular stimulation, (ii) reported only one direction of nystagmus

(equivalent to our rightward head tilt with its "climbing" sensation), and

(iii) used passive movement (the subject's chair was tilted) His findings

were different than ours in that 24 hrs of sleep deprivation yielded an 

increased response (which he accounted for by sleep deprivation having

interferred slow phase and with duration the vestibular scores. habituation process) in measures that involved

With regard to motion experiences, angular accelerations produced a slight

shortening of the duration of perceived turning across sessions for both the 

control and sleep deprived groups and had no effect on the amount of turning

for either group until the morning of Day 3 when, after 50 hrs of sleep

deprivation, the sleep deprived group showed a significant drop.

The "climbing" and "diving" experiences produced by the Coriolis stimuli

yielded patterns across sessions that were different from each other, but

similar to nystagmic responses to the same stimuli for the two groups of

subjects. Thus, the duration (slightly) and the amount (more so) of

experienced "climb" declined, while the "diving" displacement increased across

sessions and its duration showed little tendency to decline over the 50-hr

period. This resistence across sessions to reduction of the "diving". 

experience (and the accompanying nystagmus) may well relate to the compelling

nature of the "diving" sensation; that experience is much more profound than 

either the "climbing" or turning sensation and is sometimes associated with 

transient fear (of "falling") on the part of the subject. 1 

The introduction of d-amphetamine after 54 hrs of sleep deprivation produced

no clear effects on the various subjective measures of turning and Coriolis 

displacement for control subjects, but produced increments in all turning

scores and shortening of the latency of the subjective response for the sleep

deprived. Those effects suggest an influence on arousal that restores some

response for the sleep deprived but does not affect reductions (habituation)

that may be due to repeated stimulation.

The effect of d-amphetamine on nystagmus from sleep deprived subjects was to

increase all measures of the reduced responses to both angular accelerations

and Coriolis stimulation. Effects of the drug on control subjects were less

consistent. In most cases, responses continued to decline (e.g., for all 

measures of Coriolis nystagmus except fast phase responses during leftward

head movements); in other cases (e.g., for nystagmus during angular

accelerations), slight increments were obtained on some measures and

decrements on others.

These results provide no evidence for potentiation of vestibular nystagmus as

a consequence of sleep loss as proposed by Wolfe and Brown 2 That interesting

proposal, an extrapolated hypothesis from work in various fields by several

authors, 3,6,7,9,11 included the notion of a common neural mechanism involved

with Stage-1 REM (rapid eye movement) sleep and fast phase nystagmic eye

15 
movements elicited during vestibular stimulation. While there is clear

evidence that vestibular nystagmus can occur during REM stages of sleep, 9,10 

and that sleep deprivation (and, therefore, "REM deprivation") can increase

the amount of REM when sleep finally occurs, the data supporting a

potentiating effect of REM deprivation on vestibular nystagmus while suoects

are awake (but sleep deprived) were only from one of Wolfe and Brown's 1 two

* . stimuli (24 deg/sec 2 ) and not the other (8 deg/sec 2 ). Moreover, there was no

control group, and the authors discounted the idea that repetitive stimuli

* would produce anything other than a decrement in nystagmus measures; with

respect to the latter, there are data to the contrary for fast phase

responses. 2 Evidence from the present study suggests no sleep loss related

potentiation of nystagmus even for periods longer than those used by Wolfe and

Brown. 12 However, Wolfe and Brown's stimulus was considerably stronger than 

. that used in the present study and differences in findings might be related to

- the difference in stimulus levels. In any event, it is clear that

considerably more information on vestibular responsivity during sleep

deprivation is needed to provide an adequate description of the interactive

effects; to establish peripheral evidence of relationships between REM

deprivation, sleep deprivation, and fast phase vestibular eye movements; and

to define the potential effects of sleep loss in aviation environments,

particularly with respect to disorientation.

CONCLUS IONS

Ocular Nystagmus. Sleep deprivation produced a general decline in all 

measures of nystagmus produced by angular accelerations. In addition,

Coriolis (vertical) nystagmus, declined over time during head tilts

("climbing" sensations) but only for sleep deprived subjects. Ocular

responses were unaffected during movements which returned the head to an 

upright position ("diving" sensations).

d-Amphetamine increased those nystagmic responses of the sleep-deprived group 

that had declined due to sleep loss. The drug produced no reliable changes in 

responses of the control group.

Motion Experiences. Effects obtained after about 50 hrs of sleep deprivation

were generally negligible for the duration and magnitude both of left- and

right-turning sensations and of Coriolis ("climbing" and "diving")

experiences. However, a pronounced increase occurred for sleep-deprived

subjects in the latency of signaling the onset of turning experiences. This

increase suggests that performance capabilities, rather than vestibular

experiences, were most seriously affected by sleep loss: viz, reaction times were lengthened.

d-Amphetamine produced no reliable changes for the control or sleep deprived

groups in subjective vestibular responses (although measures of the turning

experiences of the sleep deprived increased somewhat), but the drug shortened

the latency (reaction time) for signals of the onset of turning by the sleep

deprived.

16
Refer enrce s

1. Collins WE. Effective Approaches to Disorientation Familiarziation

for Aviation Personnel. Washington, DC: Department of Transportation/Federal Aviation Adrninistrtaion Report No. AM-70-17,

1970.

2. Collins WE. Habituation of Vestibular Responses with and without

Visual Stimulation. In -ornhuber H-H (Ed.). andb ok of Sensory

Physiology: Vol. VI/2. New York: Springer-Verlag, 1974: 369-388. 

3. Dement WC, Greenberg S, Klein R. The Persistence of the REM

Deprivation Effect. Paper presented at the 5th Annual Meeting

of the Assoc. for the Psychophysiol. Study of Sleep.

Washington, DC: 1965.

4. Dowd PJ. Sleep Deprivation Effects on the Vestibular Habituation 

Process. J. appl. Psychol. 1974;59: 748-752.

5. Dowd PJ, Moore EW, Cramer RL. Relationships of Fatigue and Motion

Sickness to Vestibulo-ocular Responses to Coriolis Stimulation.

Hum. Factors 1975;17: 98-105. 

6. Graybiel A, Kennedy R, Guedry F, McLeod M, Colehour J, Miller E,

Knoblock E, Martz W. The Effects of Exposure to a Rotary

Environment (10 RPM) on Four Aviators for a Period of 12 Days.

In: The Role of the Vestibular Organs in the Exploration of

Space. Washington, DC: NASA, 1965: 295-338.

7. Kleitman N. Sleep and Wakefulness. Rev. ed. Chicago: Univ. Chicago

Press; 1963.

8. Ornitz EM, Forsythe AB, de la Pena A. Effects of Vestibular and

Auditory Stimulation on the REMs of REM Sleep in Autistic

Children. Arch. gen Psychiat. 1973;29: 786-791.

9. Pompeiano 0, Morrison AR. Vestibular Influences During Sleep.

Arch. Ital. Biol. 1965;103: 569-595.

10. Reding GR, Fernandez C. Effects of Vestibular Stimulation During

Sleep. EEG and Clin. Neurophysiol. 1968;24: 75-79.

11. Wendt GR. The Nature of Adaptation to Oscillatory Rotation. In:

The Role of the Vestibular Organs in the Exploration of Space.

Washington, DC:NASA, 1965; 133-139.

12. Wolfe JW, Brown JH. Effects of Sleep Deprivation on the Vestibulo- 

Ocular Reflex. Aerosp. Med. 1968;39: 947-949.

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