The influence of alcohol and sleep deprivation on stimulus evaluation

The influence of alcohol and sleep deprivation on stimulus evaluation

Alcohol, VoL 9, pp. 445--450,1992 0741-8329/92 $5.00 + .00 Copyright©1992PergamonPress Ltd. Printed in the U.S.A. All fightsreserved. RAPID COMMUNI...

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Alcohol, VoL 9, pp. 445--450,1992

0741-8329/92 $5.00 + .00 Copyright©1992PergamonPress Ltd.

Printed in the U.S.A. All fightsreserved.

RAPID COMMUNICATION

The Influence of Alcohol and Sleep Deprivation on Stimulus Evaluation K E V I N R. K R U L L , L A N D G R A V E T. S M I T H , 1 L E O N D. K A L B F L E I S C H A N D O S C A R A . P A R S O N S

The Oklahoma Center f o r Alcohol and Drug Related Research, Department o f Psychiatry and Behavioral Science, University o f Oklahoma Health Sciences Center, Oklahoma City, OK 73104 Received 5 F e b r u a r y 1992; A c c e p t e d 2 A p r i l 1992 KRULL, K. R., L. T. SMITH, L. D. KALBFLEISCH AND O. A. PARSONS. The influence of alcohol and sleep deprivation on stimulus evaluation. ALCOHOL 9(5) 445-450, 1992. - T h e effects of alcohol and sleep deprivation on choice reaction time (RT) as a function of stimulus intensity, stimulus quality, and response compatibility were investigated. Fiftyfour male subjects were assigned to one of three levels of alcohol (0.00, 0.07, or 0.10 BAC), and one of two levels of sleep deprivation (0 or 24 h). Stimulus intensity, stimulus quality, and response compatibility were varied (high or low), with RTs identified according to time on task. Significant main effects of each of the stimulus variables were present in baseline analysis, with low-level conditions producing longer RTs. Alcohol produced an overall slowing of RT. The combination of both treatments led to larger increases in RT for low stimulus quality. Sleep deprivation increased RT for high stimulus intensity. Alcohol increased RT for low stimulus intensity, but only when subjects were not sleep deprived. These results imply higher risk with degraded stimulus conditions, e.g., driving in settings of low visibility or at night. Alcohol Sleep deprivation Stimulus evaluation Response compatibility Reaction time

Stimulus intensity

P E R F O R M A N C E has been shown to decline under conditions which alter physiological states such as alcohol intoxication or sleep deprivation. Few studies have examined these decrements in performance under both conditions, even though demographic data supports the importance o f this interaction. For example, in an analysis o f U.S. Department of Transportation data, Schwing (16) reported an increased risk o f highway fatalities during the hours just after midnight, when presumably a higher degree o f sleepiness occurs. Furthermore, this risk pattern corresponded to increased blood alcohol concentration (BAC) levels in fatal accidents. Recent reports o f motor vehicle accidents also sugg#st an increased risk with sleep deprivation (7,11). Motor vehicle operation requires the processing of, and reaction to, numerous stimulus variables. When altered, these variables have the capability to influence reaction time (RT). For example, under normal conditions, increases in stimulus intensity have been shown to produce decreases in both simple and choice RT (5,8,9). Similarly, low stimulus quality or stim-

Stimulus quality

ulus degradation, has been shown to lead to increased RTs (13,14). Both of these variables are believed to affect different levels of stimulus encoding mechanisms, with stimulus intensity being processed more involuntary than stimulus quality. In terms of the response selection or reaction mechanisms, stimulus response compatibility has been shown to alter performance (13,14). Several investigations have reported that these stimulus variables produce additive effects on the reaction process. In fact, a processing pathway has been suggested, which is comprised of signal preprocessing followed by feature extraction then response selection, with stimulus intensity, stimulus quality, and response compatibility representing respective variable for this pathway (14). Impaired performance due to alcohol intoxication and sleep deprivation has been demonstrated on simple and choice RT tasks. Wilkinson and Colquhoun (22) reported reduced performance in a five choice continuous RT task due to sleep deprivation, which was reversed with exposure to low doses of alcohol. Peeke et al. (10) found increased RTs due to alcohol or sleep

This study was supported by National Institute on Alcohol Abuse and Alcoholism Grant 2ROIAA07327-05 to L. T. S. i Reprint requ~Rs should be addressed to Landgrave T. Smith, Ph.D., Oklahoma Center for Alcohol and Drug-Related Studies, 800 NE 15th Street, Suite 410, Oklahoma City, OK 73104. 445

~6 deprivation given alone but improved performance during sleep deprivation when low doses of alcohol were administered. RundeU and Williams (12) found that, when error rates are held constant, RT increased with alcohol intoxication. However, when the error rates are allowed to vary, RT increases were not observed. Smith et al. (18) found both alcohol and sleep deprivation independently slowed choice RT, however, when treatments were combined, RT decreased as error rates increased. Furthermore, a ceiling effect became apparent in that at a 0.05 BAC the effects of alcohol and sleep deprivation were additive, whereas no additional increase in RT due to sleep deprivation was apparent at a 0.08 BAC. The effect of alcohol intoxication on stimulus variables has been investigated. Alcohol has been shown to influence stimulus processing by interacting with changes in stimulus quality as opposed to response compatibility (17). This interaction takes the form of increased RT for low, as compared to high, stimulus quality conditions. In terms of stimulus intensity, Gustafson (3) reported an additive effect of stimulus intensity and alcohol ingestion on RT. In his study, 0.02% and 0.05% blood alcohol levels were representative of low and high alcohol conditions, respectively. However, in reality these levels are relatively low. Increasing blood alcohol levels may lead to an interaction between alcohol and stimulus intensity. Sleep deprivation also appears to influence stimulus evaluation. Sanders et al. (15) found sleep deprivation to interact with stimulus evaluation and not response selection, with larger increases reported for degraded as compared to undegraded stimuli. Furthermore, this effect was larger when tested in afternoon versus morning hours. When combined with alcohol intoxication and speed stress, however, sleep deprivation has been shown to produce an overall slowing of the reaction process, with no specificity for stimulus evaluation or response selection (17). Sanders and colleagnes (15) examined the influence of sleep-loss and stimulus intensity on choice RTs and found no significant interaction. They did, however, report a time-of-day effect, with larger increases in RT due to decreased intensity when subjects were run in the afternoon as compared to morning hours. These effects of alcohol and sleep deprivation may be a function of the amount of time spent on a particular task. Under periods of sustained attention or vigilance, alcohol and sleep deprivation have been found to hasten the onset of habituation, thereby increasing RT (1,2,3,6,23). Erwin and colleagues (2) reported alcohol-enhanced habituation during a 30-rain visual vigilance task. Similarly, Gustafson (3) found that under the influence of alcohol simple RT increased with time on task. Increases in RT with time on task have also been reported during periods of sleep loss (1). Deterioration in performance has been reported for sleep deprived subjects during both a visual vigilance (23) and an auditory vigilance (6) task. In both of these studies performance continued to decline as time on task proceeded. By using multiple stimulus evaluation variables, different levels of processing can be analyzed. To our knowledge, no study to date has examined the combined effects of alcohol ingestion and sleep deprivation on more than one category of stimulus evaluation mechanisms. The purpose of the present investigation was to answer the following series of questions: 1. Does alcohol and/or sleep deprivation affect stimulus evaluation? 2. If such effects exist, are they selective to mechanisms involved in the processing of stimulus intensity and/or stimulus quality?

KRULL ET AL. 3. Does one or more levels of these treatments influence response selection mechanisms? 4. Does within session fatigue or time on task either influence stimulus evaluation or modify the effects of the treatments on stimulus evaluation processes? METHOD

Subjects Fifty-four right-handed male volunteers, 21-35 years of age, were recruited from around the Oklahoma City area. Prospective subjects with neurological, medical, or psychiatric problems, extensive drug histories, or currently using medication or drugs, were rejected. Those accepted were social drinkers, with drinking patterns reported at initial screening ranging from "3-5 drinks per week" to "1-2 drinks per month." After initial screening, subjects were given a physical examination which included tests of vision and hearing and drug screening urinalyses. Eighteen subjects were assigned randomly (with the constraint of balancing across groups for age and reported drinking pattern) to each of the three intoxication levels: 0.00 BAC (placebo), 0.07 BAC, and 0.10 BAC.

Drug Treatment The ethanol treatment consisted of a mixture of commercial Everclear (95% by volume ethanol) and orange juice, served in a plastic thermos. For all treatments, including the placebo, cotton (isolated from the drink in the perforated lid assembly) was soaked in Old Crow bourbon to equate olfactory cues. Doses were placebo, 0.70 g/kg, and 1.06 g/kg ethanol, intended to give peak breath alcohol concentration (BAC) values of 0.00, 0.07, and 0.10 mg per 100 ml, representing low and moderate doses of alcohol as it is commonly used. At intervals during the experiment, the BAC values were measured using a CMI Inc. Intoxilyzer. Supplemental drinks consisting of 0.06 g/kg ethanol in the orange juice were given as required to reach and maintain the assigned BAC value.

Apparatus and Experimental Task A 2.1 × 3.1 m sound attenuated electrically shielded room was used to isolate the subject from laboratory activity during testing. Stimuli were presented with an Intelligent Systems 8001 color graphics display monitor. Experimental process control and data acquisition was accomplished with a PC Designs GV-386 microcomputer. Reaction times to visual stimuli were obtained in a task involving a finger-movement response according to the directional cue (left or right) provided by a reaction stimulus, which followed a prestimulus. Task variables included stimulus quality (STQ), stimulus-respouse compatibility (RSC), stimulus intensity (INT), and time-on-task (blocks). The reaction stimulus was a white 1 × 4 cm line drawing of an arrow on a CRT screen, with the lines two pixels in width. The arrow, pointing either left or right, was preaented inside an annulus of 7 cm dia. In the high-STQ condition, the arrow was drawn in solid lines; in the low STQ condition, a randomly selected 50~0 of the pixels comprising the arrow were scattered randomly inside the annulus. Within either STQ condition, the number of pixels, and hence the l ~ a n c e of the stimulus at a given INT level, was the same. Prior to stimulus presentation, the word "SAME" or "OPPOSITE" appeared for 750 ms to produce high and low IL_$Cconditions, respectively. After this prestimulus instruction, the screen was

A L C O H O L A N D SLEEP DEPRIVATION blank for a period o f time that was varied between 500-3000 ms, and then the arrow (reaction stimulus) was presented. Levels of STQ and RSC, as well as direction of the arrow, were balanced across trials, with order randomized. The subject began a trial with the right forefinger on a l-cm 2 central home button, with a response button 2 cm to either side. When a stimulus was presented, his task was to release the home button and press the left or right response button, corresponding to the direction in which the arrow was pointing, but with the selection modified by the prestimulus "SAME" or "OPPOSITE" RSC instruction. The subject had been practiced to respond at a speed consistent with an 8590% level o f accuracy. Stimulus intensity was varied by computer selection of one o f two resistors in parallel with the CRT brightness control. One resistor was selected to give a luminance for the stimulus of 25.6 cd/m2(high IN'T), and the other a luminance o f 3.9 cd/m~0ow INT). The INT conditions were blocked, with six blocks o f 20 trials each, three of each type. The blocks were alternated between high and low INT, and a high INT block was always presented first. The overhead lighting in the room was turned off for this experiment. Ten minutes were allowed for partial dark adaptation before the fh-st high intensity block was presented, and 5 min were allowed for partial dark adaptation at the beginning of each subsequent block of trials.

Procedure and Experimental Design One to 3 days after screening, and a practice session with the task, subjects returned to the laboratory, having been instructed to refrain from alcohol, caffeinated beverages, and other drug use for at least 48 h, as well as to get a normal night of sleep before coming in. Each subject visited the laboratory for two periods, separated by an interval of 48 or 72 h. On the first visit, there were two performance measurement sessions, 22 h apart. The first of these was a baseline session with no alcohol, conducted shortly after the subject's arrival at the laboratory at 1:00 p.m. in the afternoon. The subject then slept or remained awake, in the laboratory that night. A night technician was employed to either monitor subjects' sleep or keep the subjects awake, as appropriate. The second measurement was conducted at 1: 00 p.m. in the afternoon the next day, no less than 45 rain after alcohol or placebo treatment but after the assigned criterion BAC had been reached. A second baseline procedure was repeated 2 or 3 days later, in a fashion similar to the first session. Accordingly, there were three performance measurement sessions for each subject. Sessions 1 and 3 were baseline sessions, while the alcohol treatment was given during session 2 with half of the subjects (according to random assignment within alcohol treatment groups) sleep deprived. RESULTS

The results of this study were analyzed as follows. First, the presence of preexisting group differences, and differential group practice effects was tested for. Next, a baseline analysis was conducted to ensure adequate control over conditions. Finally, treatment effects and selective interactions of the treatments with stimulus variables were examined. In order to reduce variability treatment, data was analyzed as change from baseline measures.

Baseline Analyses Table 1 presents the results o f the baseline analysis. The lack o f a significant group main effect and the absence o f

447 TABLE 1 RESULTS OF THE REPEATED MEASURES ANALYSISOF VARIANCE FOR BASELINE DATA

Between-subjects Group Within-subjects SES BLK INT STQ RSC SES.STQ SES.RSC INT.STQ

Num. df

Den. df

F

p

2

51

0.87

0.4243

1 2 1 1 1 1 1 1

51 102 51 51 51 51 51 51

16.88 0.20 84.17 265.59 212.25 14.17 7.84 6.47

0.0001 0.8223 0.0001 0.0001 0.0001 0.0004 0.0072 0.0140

Note. Denominator df equals (if"in error for respective source. BLK = block, INT --- stimulus intensity, SES= session, STQ= stimulus quality, RSC = respons©compatibility. All main effects are depicted, in addition to all significant interactions. For simplification, nonsignificant interactions have been withheld. any group interaction with other variables suggest adequate distribution of subjects. All groups exhibited a practice effect, displaying a decrease in RT from sessions l to 3. This practice effect was not specific to any group, though levels o f certain variables tended to be selectively affected. For example, stimulus quality showed a selective practice effect, with the RT for low stimulus quality significantly decreasing from session 1 (mean = 510 ms) to session 3 (mean = 464 ms), t(106) = 2.238, p < 0.05. A selective practice effect for response compatibility was also evident. The RT for low response compatibility decreased from session l (mean = 500 ms) to session 3 (mean = 455 ms), t(106) = 2.185,p < 0.05. Main effects were present for stimulus intensity, stimulus quality, and response compatibility, but not for block (time on task). In each case, the RT associated with the low level condition was longer than that for the high level condition. Furthermore, stimulus intensity interacted with stimulus quality. At high intensity, the RT for the high stimulus quality condition (mean = 427 ms) was greater than that for the low stimulus quality condition (mean = 463 ms), t(106) = 2.039, p < 0.05. Similarly, at low intensity, the RT for the high stimulus quality condition (mean = 464 ms) was less than that for the low stimulus quality condition (mean = 510 ms), t(106) = 2.582, p < 0.01, However, the increase from high to low intensity for the high stimulus quality condition (mean = 37 ms), t(106) ffi 2.072, p < 0.05, was less than the increase for the low stimulus quality condition (mean = 47 ms), t(106) = 2.615,p < 0.01. Given the significant practice effect, the RTs for the treatment data were taken as change from a prorated baseline, which was simply the average of baseline sessions 1 and 3. Thus, a significant main effect was actually an interaction with the treatment condition. Table 2 presents the results of the change due to treatment analysis.

Treatment Effects Overall RT was increased by alcohol, but not sleep deprivation. The change in RT due to the .07 dose (mean = 57 ms) was greater than that for the 0.00 dose (mean = - 3 ms), t(106) = 3.922, p < 0.0001. Similarly, the change in RT due

~8

KRULL ET AL. TABLE 2 RESULTS OF THE REPEATED MEASURESANALYSISOF VARIANCE FOR TREATMENTDATA Num. df

Den.df

F

Between-subjects Alcohol Sleep Alcohol.Sleep

2 1 2

48 48 48

6.03 0.56 0.03

0.0046 0.4584 0.9720

Within-subjects BLK INT STQ RSC SLD,INT ALC*SLD*INT ALC,STQ,RSC ALC,SLD,INT,BLK

2 1 1 1 1 2 2 4

96 48 48 48 48 48 48 96

0.06 0.28 7.64 0.59 3.90 4.23 3.20 2.54

0.9430 0.5987 0.0081 0.4454 0.0540 0.0203 0.0497 0.0444

!intensity

p

Note. Denominator df equals df in error for respective source.

ALC = alcohol, SLD = sleep deprivation, BLK = block, INT = stimulus intensity, STQ = stimulus quality, RSC = response cornpatibility. All main effects are depicted, in addition to all significant interactions. For simplification, nonsignificant interactions have been withheld. Since change scores were utilized in the analysis of the treatment data, a significant main effect is actually an interaction with the treatment session. to the 0.10 dose (mean = 59 ms) was greater than that for the 0.00 dose, t(106) = 4.057, p < 0.0001. No significant difference existed between the 0.07 and 0.10 doses of alcohol, t(106) = 0.103,p = ns. Treatment significantly interacted with the stimulus quality variable, though this effect was not specific to the alcohol or sleep deprivation. The treatment produced a larger change in RT for the low stimulus quality condition (mean = 41 ms) than the high stimulus quality condition (mean = 34 ms). A significant interaction between stimulus quality, response compatibility, and alcohol was present, though stimulus quality did not interact with response compatibility at any of the three levels of alcohol. Instead, this interaction appears to stem from larger changes in RT due to alcohol at low stimulus quality, high response compatibility conditions. The time-on-task variable (block) did not interact with either the alcohol or the sleep deprivation treatment. Although main effects of intensity and sleep deprivation were not found, intensity interacted with sleep deprivation: with alcohol and sleep deprivation; and with alcohol, sleep deprivation, and block. For the high intensity condition, 24hour sleep deprivation produced a larger increase in RT (mean = 50 ms) compared to 0-hour sleep deprivation (mean = 26 ms), t(106) = 3.528, p < 0.001. As shown in Fig. 1, in the 0-h sleep deprivation group, the 0.07 dose of alcohol produced a larger increase in RT for the low intensity (mean = 68 ms) compared to the high intensity condition (mean = 32 ms), t(106) = 3.350, p < 0.005. This pattern was not observed in the 24-h sleep deprivation group. When analyzed across blocks, the 0-h sleep deprivation group under the 0.07 dose of alcohol displayed a decreased change in RT for the high intensity condition, and an increased change in RT for the low intensity condition as a function of time on task. Under this treatment, although the change in RT for high and low intensity did not differ when collected during the first third of the session, the decreasing and increasing trends led

i

100-

S L D = 00

/ [

-

-

High

Low

75_ "¢D -" E ..-..

5025-

[--OIT" (1) -25 .{: "~ 0O t~ rt3

.00 Blood

O 100_

h.. ,4... (1) O) ct~ c-" O

.07 Alcohol

.10 Level

S L D = 24

5O 25 0 -25 .00

Blood

.07

Alcohol

.10

Level

FIG. 1. Change in reaction time to high and low stimulus intensities as a function of sleep deprivation (SLD) and alcohol ingestion (as expressed in blood alcohol levels). Note the significant difference between high and low intensities following ingestion of the 0.07 dose in the non-sleep-deprived sample.

to a significant difference between high intensity (mean = 14 ms) and low intensity (mean = 92 ms) during the last third of the session, t(70) = 4.369,p < 0.001. Again, no such pattern was observed in the 24-h sleep-deprived group. DISCUSSION The results of the analysis of baseline data revealed adequate control over experimental variables and group assignment. As expected, additive main effects of stimulus quality and response compatibility were present, a finding which has been reported on numerous occasions (13,17,20,21). RT was slower under low compared to high intensity conditions, which was consistent with other reports (5,8,9). A significant interaction between stimulus intensity and stimulus quality did exist. Thus, in this task, stimulus quality and stimulus intensity were not processed independently. One poss~le explanation for this finding is that by decreasing the density of pixels, across the same surface area during the low stimulus quality condition, contrast was also reduced. This reduction in contrast led to a decrease in the appearance of stimulus intensity. Selective practice effects of processing of stimulus quality and response compatibility were present. Responding to the more challenging level of each of these variables was more difficult (i.e., took more time) under naive conditions. Stimu-

A L C O H O L AND SLEEP DEPRIVATION

449

lus intensity did not show this practice effect, which suggests both levels of intensity were processed efficiently or automatically. Within-session practice effects were not observed, with overall RT being similar during the beginning, middle, and end of the session. Because treatment effects were analyzed by using the change in RT from a prorated baseline, which itself was the average of pre- and postbaseline sessions, the influence of practice effects on treatment measures was controlled. As expected, based on previous findings (10,12,18), alcohol led to a global increase in RT, however, contrary to expectations, sleep deprivation did not. One possible explanation for this finding is an influence of time of day on the sleep deprivation effect. Sanders and colleagues (15) found the largest increase in RT due to sleep deprivation when subjects were tested in the afternoon compared to morning hours. The majority of subjects in the current study were run during late morning or early afternoon hours, which may not have been an optimal time of day to observe sleep deprivation effects. An alternative explanation is the large number of withinsubject repeated variables employed. Previous reports of sleep deprivation effects have either looked at habituation (1,3,4) or stimulus evaluation and response selection variables (15,17). With inclusion of all of these variables, betweensubject variance due to sleep deprivation may not be large enough to overcome within-subject variance due to repeated measures, particularly with a somewhat small sample (9 subjects per cell). Sleep deprivation did produce a progressive increase in RT at each level of alcohol intoxication (7.5 ms at 0.00 BAC, 12.5 ms at 0.07 BAC, and 17.2 ms at 0.10 BAC); however, these increases were relatively small compared to stimulus quality and stimulus intensity main effects. The average increase in RT from high to low stimulus intensity was 41.9 ms, for stimulus quality it was 41.3 ms. Stimulus intensity was influenced by both treatment conditions. When pooled across all levels of alcohol, sleep deprivation increased RT for the high stimulus intensity condition. Under periods of no sleep deprivation, mild doses of alcohol produce larger increases in RT to low vs. high intensity stimuli. With the addition of 24 hours of sleep deprivation, this same dose influenced the processing of high and low stimulus intensity to a equivalent degree. Similarly, whether sleep deprived or not, high doses of alcohol produced similar increases in RT for high and low stimulus intensities. This pattern suggests that a processing mechanism, which is sensitive to stimulus intensity, becomes saturated with either mild doses of alcohol in a fatigued individual or high doses of alcohol.

Furthermore, under this mild level of alcohol intoxication in a nonfatigued individual, the effect the alcohol has on influencing RT decreases for the high intensity condition and increases for the low intensity condition as time on task continues. This pattern can be viewed as an example of withinsession tolerance, however, it was seen in only one of the six possible treatment conditions. Whether or not this finding is specific to stimulus intensity cannot be ascertained given the interaction between intensity and quality during the baseline condition. Overall, stimulus response compatibility and time on task were not influenced by either of the treatment conditions. It may be that the prestimuli used to produce the response compatibility conditions acted as an orienting cue which, when paired with the relatively slow rate of stimulus presentation used in this particular study, produced a condition less susceptible to time-on-task effects. Treatment produced a selective effect on responses to the stimulus variables. Stimulus quality effects were influenced by the overall treatment, but not alcohol or sleep deprivation alone. The pattern of results suggests that under low stimulus quality conditions, RT is more impaired due to alcohol and sleep deprivation. The alcohol effect on stimulus quality was influenced by the level of response compatibility. Alcohol produced a larger change in RT to low stimulus quality when response compatibility was high. With low response compatibility, the change in RT due to alcohol administration was not substantially different for high compared to low stimulus quality. The current findings that the processing of stimulus quality and stimulus intensity are affected by alcohol intoxication and sleep deprivation support the notion that these treatments alter stimulus encoding mechanisms, particularly feature extraction and stimulus preprocessing. Furthermore, the effect on stimulus preprocessing increases with time on task. The absence of an interaction with stimulus response compatibility suggests that the treatment effects are selective, and do not influence mechanisms involved in response selection. The effects of alcohol and sleep deprivation on stimulus evaluation presented above have implications for human performance, particularly under degraded stimulus conditions. For example, driving during periods of poor visibility (e.g., at night or during rain storms) would involve particularly high risks following ingestion of mild doses of alcohol when sleep deprived. Similarly, ingestion of high doses of alcohol can be expected to impair performance in the sleep-deprived or rested individual under even optimum stimulus conditions.

REFERENCES 1. Dinges, D.; Powell, J. Sleepiness impairs optirdum response capability: Its time to move beyond the lapse hypothesis. Sleep Res. 18:304; 1989. 2. Erwin, C.; Wiener, E.; Linnoila, M.; Truscott, T. Alcoholinduced drowsiness and vigilance performance. J. Stud. Ale. 39: 505-516; 1978. 3. Gustafson, R. Alcohol and vigilance performance: Effect of small doses of alcohol on simple visual reaction time. Perceptual and Motor Skills 62:951-955; 1986. 4. Gustafson, R. Effect of small doses of alcohol and signal intensity on simple auditory reaction time in a monotonous test situation. Perceptual and Motor Skills 63:539-543; 1986. 5. Keuss, P.; Van der Molen, M. Positive and negative effects of stimulus intensity in auditory reaction tasks: Further studies on immediate arousal. Acta Psychologica 52:61-72; 1982. 6. Lisper, H.; Kjellberg, A. Effects of 24-hour sleep deprivation on

7. 8. 9. I0. l I. 12.

rate of decrement in a lO-minute auditory reaction time task. J. Exp. Psychol. 96:287-290; 1972. Milter, M.; Carskadon, M.; Czeisler, C.; Dement, W.; Dinges, D.; Graeber, R. Catastrophes, sleep, and public policy: Consensus report. Sleep II:I00-I09; 1988. Niemi, P. Stimulus intensity effects on auditory and visual reaction processes. Acta Psychologica 43:299-312; 1979. Niemi, P.; Lehtonen, E. Foreperiod and visual stimulus intensity: A reappraisal. Acta Psychologica 50:73-82; 1982. Peeks, S.; Callaway, E.; Jones, R.; Stone, G.; Doyle, J. Combined effects of alcohol and sleep deprivation in normal young adults. Psychopharmacology 67:279-287; 1980. Roth, T.; Roehrs, T. Sleepiness and motor vehicle accidents. Int. Clin. Psychopharmacol. 3:11l-116; 1988. Rundell, O.; Williams, H. Alcohol and speed-accuracy trade-off. Hum. Factors 21:433--443; 1979.

450 13. Sanders, A. F. Stage analysis of reaction process. In: Stelmach, G. E.; Requin, J., eds. Tutorials in motor behavior. Amsterdam: North Holland; 1980. 14. Sanders, A. F. Structural and functional aspects of the reaction process. In: Dornic, S., ed. Attention and performance, VI. Hillsdale, NJ: Erlbaum; 1977. 15. Sanders, A.; Wijnen, J.; Arkel, A. An additive factor analysis of the effects of sleep loss on reaction process. Acta Psycholngica 51:41-59; 1982. 16. Schwing, R. Exposure-controlled highway fatality rates: Temporal patterns compared to some explanatory variables. Alcohol, Drugs and Driving 6:275-285; 1990. 17. Smith, L.; Idirisi, A.; Sinha, R.; Parsons, O. The interaction of alcohol and sleepdeprivation with stimulus quality and speed stress in a choice reaction time task. (unpublished manuscript; 1992).

KRULL ET AL. 18. Smith, L.; Sinha, R.; Williams, H. The interaction of alcohol and sleep deprivation in two reaction time tasks. Alcohol, Drugs and Driving 6:341-350; 1990. 19. Sternberg, S. Memory scanning: Mental processes revealed by reaction time experiments. Am. Scientist 57:421-457; 1969. 20. Sternberg, S. Memory scanning: New findings and current controversies. Q. J. Exp. Psych. 27:1-32; 1975. 21. Taylor, D. A. Stage analysis of reaction time. Psychol. Bull. 83: 161-191; 1976. 22. Wilkinson, R.; Calquhoun, W. Interaction of alcohol with incentive and with sleep deprivation. J. Exp. Psychol. 76:623-629; 1968. 23. Williams, H.; Kearney, O.; Lubin, A. Signal uncertainty and sleep loss. J. Exp. Psychol. 69:401--407;1965.