Sleep deprivation may be undermining teen health

Lack of sufficient sleep--a rampant problem among teens--appears to put adolescents at risk for cognitive
and emotional difficulties, poor school performance, accidents and psychopathology, research suggests.

By SIRI CARPENTER
Monitor Staff
October 2001, Vol 32, No. 9
Print version: page 42

On any given school day, teen-agers across the nation stumble out of bed and prepare for the day. For most, the
alarm clock buzzes by 6:30 a.m., a scant seven hours after they went to bed. Many students board the school bus
before 7 a.m. and are in class by 7:30.

In adults, such meager sleep allowances are known to affect day-to-day functioning in myriad ways. In adolescents,
who are biologically driven to sleep longer and later than adults do, the effects of insufficient sleep are likely to be
even more dramatic--so much so that some sleep experts contend that the nation's early high-school start times,
increasingly common, are tantamount to abuse.

"Almost all teen-agers, as they reach puberty, become walking zombies because they are getting far too little sleep,"
comments Cornell University psychologist James B. Maas, PhD, one of the nation's leading sleep experts.

There can be little question that sleep deprivation has negative effects on adolescents. According to the National
Highway Traffic Safety Administration, for example, drowsiness and fatigue cause more than 100,000 traffic
accidents each year--and young drivers are at the wheel in more than half of these crashes.

Insufficient sleep has also been shown to cause difficulties in school, including disciplinary problems, sleepiness in
class and poor concentration.

"What good does it do to try to educate teen-agers so early in the morning?" asks Maas. "You can be giving the most
stimulating, interesting lectures to sleep-deprived kids early in the morning or right after lunch, when they're at their
sleepiest, and the overwhelming drive to sleep replaces any chance of alertness, cognition, memory or
understanding."

Recent research has also revealed an association between sleep deprivation and poorer grades. In a 1998 survey of
more than 3,000 high-school students, for example, psychologists Amy R. Wolfson, PhD, of the College of the Holy
Cross, and Mary A. Carskadon, PhD, of Brown University Medical School, found that students who reported that they
were getting C's, D's and F's in school obtained about 25 minutes less sleep and went to bed about 40 minutes later
than students who reported they were getting A's and B's.

In August, researchers at the University of Minnesota reported the results of a study of more than 7,000 high-school
students whose school district had switched in 1997 from a 7:15 a.m. start time to an 8:40 a.m. start time. Compared
with students whose schools maintained earlier start times, students with later starts reported getting more sleep on
school nights, being less sleepy during the day, getting slightly higher grades and experiencing fewer depressive
feelings and behaviors.

Also troubling are findings that adolescent sleep difficulties are often associated with psychopathologies such as
depression and attention deficit hyperactivity disorder (ADHD).

This research, combined with studies showing widespread sleep deprivation among teens, has propelled efforts to
educate children and adults about the importance of a good night's sleep and to persuade schools to push back high-
school starting times.

"There is substantial evidence that the lack of sleep can cause accidents, imperil students' grades and lead to or
exacerbate emotional problems," says U.S. Rep. Zoe Lofgren (D-Calif.), who has introduced a bill that would provide
federal grants to help school districts defray the cost of pushing back school starting times. Adjusting school
schedules, Lofgren says, "could do more to improve education and reduce teen accidents and crime than many more
expensive initiatives."

The research has also spurred further investigations into why teens need extra sleep, the effects of sleep deprivation
on cognition, emotion regulation and psychopathology, and the long-term consequences of chronic sleep deprivation.

Dogma reversed

For decades, experts believed that people require less sleep as they move from infancy through adulthood.

It's easy to see why this belief persisted: Adolescents sleep less than they did as children, declining from an average
of 10 hours a night during middle childhood to fewer than 7.5 hours by age 16. According to Wolfson and
Carskadon's 1998 study, 26 percent of high school students routinely sleep less than 6.5 hours on school nights, and
only 15 percent sleep 8.5 hours or more. The same study indicated that to make up for lost sleep, most teens snooze
an extra couple of hours on weekend mornings--a habit that can lead to poorer-quality sleep.

But to researchers' surprise, in the past two decades studies have shown that teen-agers require considerably more
sleep to perform optimally than do younger children or adults. Starting around the beginning of puberty and
continuing into their early 20s, Carskadon and colleagues have shown, adolescents need about 9.2 hours of sleep
each night, compared with the 7.5 to 8 hours that adults need.

In addition to needing more sleep, adolescents experience a "phase shift" during puberty, falling asleep later at night
than do younger children. Researchers long assumed that this shift was driven by psychosocial factors such as social
activities, academic pressures, evening jobs and television and Internet use. In the past several years, however,
sleep experts have learned that biology also plays a starring role in adolescents' changing sleep patterns, says
Carskadon.
Indeed, Carskadon's research is greatly responsible for that new understanding. In a pair of groundbreaking studies
published in 1993 and 1997, she and colleagues found that more physically mature girls preferred activities later in
the day than did less mature girls, and that in more physically mature teens, melatonin production tapered off later
than it did in less mature teens. Those findings, Carskadon says, suggest that the brain's circadian timing system--
controlled mainly by melatonin--switches on later at night as pubertal development progresses.

Changes in adolescents' circadian timing system, combined with external pressures such as the need to awaken
early in the morning for school, produce a potentially destructive pattern of early-morning sleepiness in teen-agers,
Carskadon argues. In a laboratory study of 40 high-school students published in the journal Sleep (Vol. 21, No. 8) in
1998, she, Wolfson and colleagues examined the effect of changing school starting times from 8:25 a.m. to 7:20 a.m.

Their results were disturbing: Almost half of the students who began school at 7:20 were "pathologically sleepy" at
8:30, falling directly into REM sleep in an average of only 3.4 minutes--a pattern similar to what is seen in patients
with narcolepsy.

Those findings, says Carskadon, persuaded her that "these early school start times are just abusive. These kids may
be up and at school at 8:30, but I'm convinced their brains are back on the pillow at home."

Elusive questions

The evidence of adolescents' increased need for sleep and that many--if not most--teen-agers are chronically sleep
deprived has raised further questions. Particularly elusive, says Carskadon, has been the question of why
adolescents' circadian clocks shift to a later phase around the beginning of puberty.

One possibility, she believes, is that the brain's sensitivity to light changes during adolescence. At the annual meeting
of the Associated Professional Sleep Societies in June, she and colleagues presented research showing that in the
evening, exposure to even very dim lighting delayed melatonin secretion for participants who were in middle or late
puberty, but not for prepubertal participants.

Carskadon is also interested in how teen-age alcohol use might affect the brain's sleep system. Following up on
studies in adults that have established a link between drinking problems and changes in sleep patterns, for example,
she and her colleagues plan to examine whether during early development, young people with a family history of
problem drinking might have abnormalities in the brain mechanisms that govern sleep.

Just as important as the question of why sleep patterns change during adolescence is the issue of how sleep
deprivation influences adolescents' emotion regulation and behavior. Many researchers have noted that sleep-
deprived teen-agers appear to be especially vulnerable to psychopathologies such as depression and ADHD, and to
have difficulty controlling their emotions and impulses.

Although it's difficult to untangle cause and effect, it's likely that sleep deprivation and problems controlling impulses
and emotions exacerbate one another, leading to a "negative spiral" of fatigue and sleepiness, labile emotions, poor
decision-making and risky behavior, says Ronald E. Dahl, MD, a professor of psychiatry and pediatrics at the
University of Pittsburgh.

Despite the evidence that insufficient sleep affects young people's thinking, emotional balance and behavior, the
long-term effects of chronic sleep deprivation on learning, emotion, social relationships and health remain uncertain.

"There's a real need for longitudinal studies to follow through later childhood and adulthood," says psychologist Avi
Sadeh, PhD, a sleep researcher at Tel Aviv University. Although research has amply demonstrated that sleep
problems affect young people's cognitive skills, behavior and temperament in the short term, he says, "It's not at all
clear to what extent these effects are long-lasting."

Researchers push for school changes, public outreach

With such a wealth of evidence about the prevalence of adolescent sleep deprivation and the risks it poses, many
sleep researchers have become involved in efforts to persuade school districts to push back high-school starting
times so that teens can get their needed rest.

Some schools argue that adjusting school schedules is too expensive and complicated. But others have responded
positively to sleep experts' pleas. The Connecticut legislature is considering a bill that would prohibit public schools
from starting before 8:30 a.m., and Massachusetts lawmakers are also weighing the issue. And Lofgren's "Zzzzz's to
A's" bill, first introduced in the U.S. House of Representatives in 1998, would provide federal grants of up to $25,000
to school districts to help cover the administrative costs of adjusting school start times.

These efforts are a move in the right direction, says Wolfson. But, she says, changing school start times isn't the
entire answer. "I think we have to be educating children, parents and teachers about the importance of sleep, just as
we educate them about exercise, nutrition and drug and alcohol use."

Toward that end, several public-education efforts are now under way:

 With a grant from the Simmons mattress company, Cornell's Maas recently produced a film on teen-age
sleep deprivation, its consequences and the "golden rules" for healthy sleep. The film is scheduled for
distribution through parent-teacher associations and school principals this fall. In August, Maas also
published a children's book, "Remmy and the Brain Train," which discusses why the brain requires a good
night's sleep.
 Next year, the National Center for Sleep Disorders Research at the National Institutes of Health plans to
release a supplemental sleep curriculum for 10th-grade biology classes, addressing the biology of sleep, the
consequences of insufficient sleep and the major sleep disorders. In a related effort, the center is
coordinating a sleep-education campaign aimed at 7- to 11-year-olds.
 Wolfson and colleague Christine A. Marco, PhD, a psychologist at Worcester State College, are pilot-testing
an eight-week sleep curriculum for middle-school students. As part of the curriculum, students keep sleep
diaries, play creative games and participate in role-playing about sleep, and set goals--for example, for the
 amount of sleep they want to get or for regulating their caffeine intake. Preliminary results indicate that the
curriculum helps students improve their sleep habits.

"Changing school start times is one critical measure we can take to protect young people's sleep," says Wolfson.
"And then, if we can only understand what's going on with sleep in these sixth-, seventh- and eighth-graders, we can
intervene to change their sleep behavior before it gets out of hand."
Sleep deprivation can look like ADHD
Jason Williams
Psychology Today; Aug 2003; 36, 4; ProQuest Psychology Journals
pg. 23

Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.
Impact of daytime sleepiness underrated
Sharpley, Ann
The Lancet; Jul 13, 1996; 348, 9020; ProQuest Psychology Journals
pg. 71
Psychonomic Bulletin & Review
2009, 16 (4), 742-751
doi:10.3758/PBR.16.4.742

Sleep deprivation affects multiple

distinct cognitive processes
Roger Ratcliff
Ohio State University, Columbus, Ohio
and

Hans P. A. Van Dongen

Washington State University, Spokane, Washington

Sleep deprivation adversely affects the ability to perform cognitive tasks, but theories range from predicting an
overall decline in cognitive functioning (because of reduced stability in attentional networks) to claiming specific
deficits in executive functions. In the present study, we measured the effects of sleep deprivation on a two-choice
numerosity discrimination task. A diffusion model was used to decompose accuracy and response time distribu-
tions in order to produce estimates of distinct components of cognitive processing. The model assumes that, over
time, noisy evidence from the task stimulus is accumulated to one of two decision criteria and that parameters
governing this process can be extracted and interpreted in terms of distinct cognitive processes. The results showed
that sleep deprivation affects multiple components of cognitive processing, ranging from stimulus processing to pe-
ripheral nondecision processes. Thus, sleep deprivation appears to have wide-ranging effects: Reduced attentional
arousal and impaired central processing combine to produce an overall decline in cognitive functioning.

Sleep deprivation is a manipulation that allows arousal
levels to be manipulated to a higher degree than one sees
in the experimental interventions typically used in cogni-
tive research. The effects of acute sleep deprivation on
cognition are reversible, so sleep deprivation represents
a different approach for investigating the underlying pro-
cesses of cognition. Conversely, carefully selected tests of
cognitive processing can provide new information about
the effects of sleep deprivation on the brain.
Experimental and modeling studies of the effects of
sleep deprivation on cognitive performance have thus far
focused almost exclusively on global outcome measures
(Durmer & Dinges, 2005; Van Dongen, 2004). Such re-
search has revealed that overall performance declines as
a function of time spent awake, modulated by circadian
rhythm (Van Dongen & Dinges, 2005). However, not much
is known about the effects of sleep deprivation on detailed
performance outcomes, such as response time (RT) distri-
butions, or on changes in specific cognitive components,
such as decision processes. Attempts are being made to
bridge this gap with the use of computational modeling
that is based on cognitive architectures (Gunzelmann,
Gluck, Price, Van Dongen, & Dinges, 2007), but these
efforts need to be informed by precise information regard-
ing which component processes of cognition are affected
by sleep deprivation and how.
The present study addressed this issue. Participants
were tested on a two-choice numerosity discrimination
task at baseline after 57 h of sleep deprivation and again
following 2 days with recovery sleep. Participants in a
control group were tested at the same times, but without
sleep deprivation. In each trial of the two-choice task, be-
tween 31 and 70 asterisks were placed in random positions
in a 10 3 10 array, and the participants were instructed to
judge whether the number was greater than 50 (large) or
less than 50 (small ). This task was selected because it has
few memory demands or perceptual limitations (such as
brief presentation or low contrast), allowing us to focus on
central cognitive processes and decision processes.
We applied the diffusion model (Ratcliff, 1978, 1988;
Ratcliff, Cherian, & Segraves, 2003; Ratcliff & Mc­Koon,
2008; Ratcliff & Smith, 2004; Ratcliff, Van Zandt, &
McKoon, 1999; Smith, 2000; Smith, Ratcliff, & Wolf-
gang, 2004; Voss, Rothermund, & Voss, 2004) to the data
from each individual participant. From this, we were able
to obtain estimates of the model parameter values for the
baseline, deprivation, and recovery sessions in the experi-
mental group, as well as for those in the control group.
These parameter estimates allowed us to draw conclusions
about the effects of sleep deprivation on components of
cognitive processing.
Method
Participants
A total of 25 participants (13 women; age range, 22–38 years)
completed the study. The participants were screened with physical
examinations, urine and blood chemistry tests, and questionnaires
to ensure they were physically and psychologically healthy and free

R. Ratcliff, ratcliff.22@osu.edu

© 2009 The Psychonomic Society, Inc. 742

 Sleep Deprivation Effects on Cognitive Processes     743
of traces of drugs. They were good sleepers (getting between 6 and
10 hours per night), reported themselves as being neither extreme
morning nor extreme evening types, and had no sleep or circadian
disorder (including normal baseline polysomnogram). They had
not traveled between time zones in the prior 3 months and had not
worked shifts in the prior month. The participants were required to
maintain their habitual sleep schedule in the week before the study,
as monitored by sleep/wake logs, time-stamped voice recordings of
bedtimes and rising times, and wrist actigraphy (wrist-worn activ-
ity monitoring). They had normal or corrected-to-normal vision.
The study was approved by the Institutional Review Board of Wash-
ington State University, and all of the participants gave written in-
formed consent.
Design
The participants were in the lab for 6 consecutive nights (7 days).
They were randomized to either a sleep-deprivation condition
(12 participants) or a control condition (13 participants). On Days 1
and 2, all of the participants had baseline sleep (10 h in bed each
night). They practiced the numerosity discrimination task for 10 min
twice on Day 1. On Day 3, participants in the experimental condition
began 62 h of continuous wakefulness. At 17:00 on that day, while
9 h awake, they took their baseline test. Two days later, at 17:00,
while 57 h awake (48 h after Test 1), they took their second test. After
the 62 h of wakefulness, participants were allowed 2 recovery nights
(10 h in bed each night). At 17:00 on the last day (48 h after Test 2),
they took their recovery test. The control participants were tested at
the same times but had sleep (10 h in bed) each night throughout the
study. Participants continually stayed inside the isolated, environ-
mentally controlled laboratory during the study and were behavior-
ally monitored at all times by trained research assistants.
Procedure
Cognitive performance was tested on a two-choice numerosity
discrimination task. On each trial, a number of asterisks between 31
and 70 was generated and placed in random positions in a 10 3 10
array of blank characters in the upper left-hand corner of an LCD
monitor (from a viewing distance of 57 cm, the width of the asterisk
array was 4º, and the height was 9º). Varying the number of asterisks
causes performance accuracy to vary from near-ceiling (100% ac-
curate) to near-floor (50% accurate) levels, providing a full range
of values for this dependent variable for the purpose of modeling.
They were clearly visible, light characters presented against a dark
background. The participants were asked to press the “/” key if the
number of displayed asterisks was judged to be large and the “z”
key if the number was judged to be small. Each test array remained
on the screen until a response was made. “Small” responses to ar-
rays of 31 to 50 asterisks and “large” responses to arrays of 51 to
70 asterisks were counted as correct. Feedback on the accuracy of a
response was provided by displaying the word “error” or “correct,”
as appropriate, on the screen for 500 msec after each response was
made. There were 30 blocks of 40 trials (all the numbers of asterisks,
from 31 to 70) per test session. The participants were instructed to
respond quickly and accurately, but not so quickly that they would
hit the wrong key. The participants were also informed that they
could take a break between blocks of trials. Examples of large and
small numbers of asterisks were shown before the session to provide
participants with a reference.
Results
Summaries of the accuracy and RT data for the experi-
mental and control groups for the three sessions are shown
in Figure 1. Responses from the first block of each ses-
sion, short (,280 msec) and long (.5,000 msec) outlier
RTs in all blocks (less than 1.7% of the data in the sleep-
deprivation session and less than 0.2% of the data for the
other sessions), and the first response in each block were
eliminated. The left-hand panels show the proportion of
“large” responses as a function of eight numerosity cat-
egories representing eight groups of numbers of asterisks
(31–35, 36– 40, 41– 45, 46–50, 51–55, 56–60, 61–65,
66–70), and the right-hand panels show mean RT for
“large” and “small” responses, as a function of the number
of asterisks. Response proportions were very similar for
the experimental and control groups in the baseline and
recovery sessions; but in the sleep-deprivation session,
the experimental participants showed a loss of accuracy,
as compared with the control participants’ accuracy lev-
els. In the baseline session, RTs from the experimental
and control groups were similar. In the sleep-deprivation
session, the experimental group exhibited mean RTs
over 200 msec longer than those exhibited by the control
group. In the recovery session, the experimental group had
slightly slower responses than those by the control group,
but performance was almost back to baseline levels. These
results are consistent with the documented overall effects
of sleep deprivation on cognitive performance (Durmer &
Dinges, 2005; Van Dongen & Dinges, 2005).
Diffusion Model
The diffusion model is designed to explain the cogni-
tive processes involved in making simple two-choice deci-
sions. The model separates the quality of evidence enter-
ing a decision from the decision criteria, as well as from
nondecision processes. Decisions are assumed to be made
by a noisy process that accumulates information over time,
from a starting point z toward one of two response criteria,
or boundaries: a and 0 (Figure 2). When a boundary is
reached, a response is initiated. The rate of accumulation
of information is called the drift rate (v), and it is deter-
mined by the quality of the information extracted from
the stimulus in perceptual tasks and the quality of match
between the test item and memory in lexical decision and
memory tasks. The mean of the distribution of times taken
up by the nondecision component (the combination of en-
coding, response execution, etc.) is labeled Ter . Within-
trial variability (Gaussian-distributed noise) in the accu-
mulation of information from the starting point toward the
boundaries results in processes with the same mean drift
rate terminating at different times (producing RT distribu-
tions) and, sometimes, terminating at the wrong boundary
(producing errors).
The values of the components of processing are as-
sumed to vary from trial to trial, under the assumption
that participants cannot accurately set the same param-
eter values from one trial to another (e.g., Laming, 1968;
Ratcliff, 1978). Across-trial variability in drift rate is
normally distributed with SD h, across-trial variability in
starting point is uniformly distributed with range sz , and
across-trial variability in the nondecision component is
uniformly distributed with range st . This across-trial vari-
ability allows the model to fit the relative speeds of correct
and error responses (Ratcliff et al., 1999). In signal detec-
tion theory, which deals only with accuracy, all sources
of across-trial variability would be collapsed onto one
parameter—namely, variability in evidence across trials.
In contrast, in diffusion model fitting, the separate sources
744    Ratcliff and Van Dongen

1 = sleep-deprived, “large” responses

2 = control, “large” responses
1 = sleep-deprived group 3 = sleep-deprived, “small” responses
2 = control group 4 = control, “small” responses

1.0 1
2
“Large” Response Proportion

Mean Response Time (msec)

2 1
1
1,000
.8

Baseline Session
2
1
.6 800 2 1 4
3
1 2
3
4 3
1
2
3
4 1
.4 2 4
2
1 3
4 1
600 3 2
4 2
1
.2
2
1
2
1 2
1 400
0

1.0 2 2
“Large” Response Proportion

Mean Response Time (msec)

2 1 1
1 1,000 3
1 3

Deprivation Session
.8 1 1
2 3 3 1
3
1 1
.6 3
800 2 4 1
4
2 4
1 2
.4 4
2 2
600 4 2
1 4 2
.2 1
1 2
2 2 400
0
1.0 2 2
1
“Large” Response Proportion

Mean Response Time (msec)

2 1
1 1,000
.8

Recovery Session
2
1
.6 800 1
1 3 4
2 3
2 4
1
4 2 3
.4 3 1
2
1 4 2
600 3
4 1
3
4 2 1
.2 2
1
2
2
1 2
1 400
0
33 38 43 48 53 58 63 68 33 38 43 48 53 58 63 68

Mean Number of Asterisks Mean Number of Asterisks

Figure 1. Accuracy and mean response time (RT), as a function of numerosity category for the three
sessions and two participant groups. Note that mean error RTs for the two extreme numerosity cat-
egories are not plotted; there were some participants with zero error responses in those categories.

Correct RT distribution
“A” decision criterion
a correct correct
response ate v response
Drift r
Evidence

z
Time

error
response
0
“B” decision criterion
Error RT distribution
Figure 2. Illustration of the diffusion model with starting point z,
boundary separation a, and drift rate v. Three sample paths are
shown, illustrating variability within the decision process, and cor-
rect and error response time (RT) distributions are illustrated.
 Sleep Deprivation Effects on Cognitive Processes     745
of across-trial variability are identified. Thus, if simulated
data are fit by the model, then, for example, variability
in drift rate is not incorrectly recovered as variability in
starting point (Ratcliff & Tuerlinckx, 2002). The success
of parameter identifiability comes partly from the require-
ment that the model is fit to both the correct and the error
RT distributions, which provide very tight constraints on
the model (see Ratcliff, 2002).
In almost all RT studies (e.g., Ratcliff, 1979, 1993),
some proportion of responses are spurious contaminants,
which have previously been explicitly modeled in ap-
plications of the diffusion model (Ratcliff & Tuerlinckx,
2002) as random delays in processing. Thus, predicted
RTs are mixtures of pure diffusion model processes and
diffusion model processes with a delay added (usually
0%–2%), which means that contaminant processes are
just as accurate as processes without contaminants. In
this application, we used the simplest alternative assump-
tion we could by representing contaminants as random
guesses (Vandekerck­hove & Tuerlinckx, 2007) that were
uniformly randomly distributed over the range from the
shortest to the longest RT for each numerosity category.
Thus, the predicted RT distribution is a probability mix-
ture of diffusion model processes and random guesses.
Random guesses can be distinguished from the assump-
tion of an added random delay because random guesses
reduce accuracy, as was shown in the sleep-deprivation
data. Unlike the assumption of random delays added to
diffusion model RTs, the assumption of random guesses
means that these processes are outside the diffusion model
processing assumptions. Although it may seem that this
assumption provides a lot of model freedom, no additional
model parameters are added beyond the proportion of
contaminants, and the ability of the mixture to account for
RT distributions (discussed below) supports the assump-
tion. Note that recovery of diffusion model parameters is
reasonably robust to the assumed form of the contami-
nant distribution; for example, if exponentially distributed
contaminants are simulated and the recovery program as-
sumes uniformly distributed contaminants, the model pa-
rameters are recovered well (Ratcliff, 2008).
The diffusion model was fit to the accuracy and RT
distributions using a standard chi-square method (Ratcliff
& Tuerlinckx, 2002). The values of all of the parameters,
including the variability parameters, are estimated simul-
taneously from the data by fitting the model to all of the
conditions of an experiment. It was assumed that “large”
responses to large stimuli were symmetric with “small”
responses to small stimuli; that is, drift rates were equal,
but with opposite signs. Thus, there were four distinct
drift-rate parameters (v1–v4) for the eight numerosity cat-
egories. However, participants can have a bias in the zero
point of drift, so a drift criterion, vc (analogous to the cri-
terion in signal detection theory), was added to each drift
rate (Ratcliff & McKoon, 2008). Because the values for
the drift rate parameter for the two middle, most difficult
numerosity categories (i.e., v4, for 46–50 and 51–55 as-
terisks) were small and variable, they were not used in our
statistical analyses; but they did help constrain the model
fits. All of the parameters of the model (except drift rate)
were kept constant across numerosity categories in each
session, because it is routinely assumed that participants
cannot change their decision criteria or adjust the dura-
tion of other components of processing as a function of
the quality of the stimulus being presented. All of the pa-
rameters of the model were allowed to vary between ses-
sions, because practice could alter any of the parameters.
The model can be seen as decomposing accuracy and RT
data for correct and error responses into distinct cognitive
processes.
Fits of the Diffusion Model
To display the data and the diffusion model fits, we com-
puted the average over participants for quantile RTs (see
Figure 3A) and for the proportion of “large” and “small”
responses as a function of the numerosity categories. We
also averaged the parameter estimates over participants and
computed the corresponding model predictions; we then
generated the quantile probability functions. To display the
quality of fit of the model to the data, Figure 3B shows
the observed and predicted quantile RTs (vertical) and
the proportion of “large” and “small” responses (horizon-
tal), as a function of the number of asterisks (numerosity
categories) presented. These graphs contain information
about all of the data and model predictions of the experi-
ment: the probabilities of correct and error responses and
the shapes of the RT distributions for both correct and error
responses. As Figure 3B shows, the probability of a “large”
response varied from near 1 for stimuli with large numbers
of asterisks to near 0 for stimuli with small numbers of
asterisks (cf. Figure 1). Median RT increased for the more
difficult stimuli (numbers of asterisks close to 50), with
most of the slowing coming from the skewing of the RT
distributions, because the .9 quantile RTs increased much
more than did the .1 quantile RTs.
Parameter Estimates
The average model parameter estimates are shown in
Table 1 and plotted in Figure 4, as a function of session
and experimental versus control groups. For the sleep-
deprivation session, relative to the baseline and recovery
sessions and to the control group, boundary separation in-
creased, drift rates decreased, variability in starting point
and nondecision components increased, and the propor-
tion of contaminants increased.
The parameter values represent the behavior of com-
ponents of processing in the experiment, and we used
their values to interpret the effects of sleep deprivation on
performance in the two-choice task. Two-way mixed ef-
fects ANOVAs of each of the parameters for the three ses-
sions 3 experimental and control groups were performed;
the results are shown in the Table 2 note. Table 2 shows
planned statistical comparisons between the experimental
group and the control group, as well as between the sleep-
deprivation session and the baseline and recovery sessions.
For the baseline and recovery sessions, there were almost
no significant differences between the experimental and
control groups. For all comparisons between the sleep-
deprivation session and the corresponding control session
and for all comparisons between the sleep-deprivation
746    Ratcliff and Van Dongen

A 5

Probability Density
4

Quantiles .005 .1 .3.5 .7 .9 .995

B
“Large” Responses “Small” Responses “Large” Responses “Small” Responses
RT Quantile (msec)

1,500
o o o o o o o xo
o x o o x xo x o xo
x o ox o
o o o x
1,000 xo ox ox o o xo
o ox
ox o
o xo xo o ox o xo
o xo xo xo o x ox xo o o xo xo
oxox xo ox ox xo xo oo ox xo ox xo ox o ox ox xo x xo xo xo
ox xo xo oxox xo oxx xxo o ox xo oo xo xoo
oo o ox oxo
xo xxo o xo o oxxxo
o oox o ox ox ox
ox xo
x xxo oo
o
xx o
xo xxo
o xxxxxoo
500 oo
o o ox ox xo xoxxxo
o
oo
o xo xo ox xxooxo o o
oo o ox ox oxxoxxo
o
o
o oo xo xo xo xxo oo
o
Experimental Session 1 Experimental Session 1 Control Session 1 Control Session 1

oo o x
ox o
oxox ox x xx x
o x xo x x
RT Quantile (msec)

1,500 x
o o x
x
o o
o ox o xo xo
oo o ox
ox o x xo o o
1,000 oxox ox
ox x o o o xo
ox x o x xo o o xo o xo
oo ox
ox ox ox ox oxxo x xo xo ox o xo xo
oxox x xx x o xo xoxo o xo xo oo ox xo xo xoxo
o ox o
x x oxxo o o
x x x o xo xoxxo oxx ox ox ox xo xo xo
xo xxo
xox o
oxx ox oxxxo o o o ox ox o
xxxo
o xxo xo
xxxo
o
oxx o
o xo o xoxxxo
o
500 oo ox ox xxo
ox ox oo oxxo xo xo x o xo xx
oo oo
ooo ox ox xoo o
o oo o xo xo xo xxo
oxoo
Experimental Session 2 Experimental Session 2 Control Session 2 Control Session 2
RT Quantile (msec)

1,500
o ox o xo
o x o x ox xo
ox o o
o o o ox xo
1,000 ox o
xo ox xo o xo o
xo xo
o ox xo o xo
oxx o ox ox ox oo xo xo xo
o xo ox ox xo xo o o xo xo ox o ox o ox xo xoxo o ox xo xoxoxo
xxo x
o xo ox ox xo xxxo
o o
xxo oo
xx ox xo xo ox oxxxo o ox
ox
xo xxo oxox o xo xo
xo xxo o
xoxxxo
o ox xo
xo oo oxx o xxo xo
ooo ox oxxo oo o o
500 oo o ox xo xxo
o o oo o xo xo o o
oxxxo
o o
oo o ox ox xxo
o xxo o
oxxo
o o
oo xo xo xoxxo
oxoo
Experimental Session 3 Experimental Session 3 Control Session 3 Control Session 3

0 .2 .4 .6 .8 1.0 0 .2 .4 .6 .8 1.0 0 .2 .4 .6 .8 1.0 0 .2 .4 .6 .8 1.0

Response Proportion Response Proportion Response Proportion Response Proportion

Figure 3. Response time (RT) quantiles and response proportions. Panel A shows an RT distribution histogram (the circles joined by
lines), with the quantile RTs identified on the abscissa and as rectangles with .2 area between the .1, .3, .5 (median), .7, and .9 quantiles
and .095 area between extremes, the .005 and .1 quantiles and the .9 and .995 quantiles (we use .005 and .995 for illustration as being
a little less variable than the maximum and minimum). Panel A shows that the six rectangles between and outside the five quantiles
approximate the density function rather well. Panel B shows quantile probability functions for “large” and “small” responses for the
three sessions in the experimental group (Session 1 baseline, Session 2 sleep-deprived, and Session 3 recovery) and in the control group.
The quantile RTs in each vertical line of Xs from the bottom to the top are the .1, .3, .5 (median), .7, and .9 quantiles, respectively. The
Xs represent the data, and the Os joined with lines represent the predicted quantile RTs from the diffusion model. The eight columns
of Xs in each graph are for eight different stimulus categories—namely, 31–35, 36–40, 41–45, 46–50, 51–55, 56–60, 61–65, and 66–70
asterisks for “large” responses; for “small” responses, the columns of Xs are for the same eight stimulus categories, but in the opposite
order. The horizontal position of the columns of Xs indicates the response proportion for that category. Note that extreme error quan-
tiles could not be computed for some of the numerosity categories because there were too few errors for some participants, so only the
median RT value is plotted.
 Sleep Deprivation Effects on Cognitive Processes     747

Table 1
Parameter Values Averaged Over Participants
Session a Ter η sz v1 v2 v3 v4 po st vc z χ2
Experimental Group
  Baseline .151 .428 .171 .066 .546 .416 .271 .093 .003 .138   .007 .075 101
  Sleep-deprived .189 .401 .216 .130 .403 .318 .198 .083 .101 .165   .011 .089 163
  Recovery .151 .420 .209 .083 .615 .491 .308 .110 .001 .113   .005 .076 101
Control Group
  Baseline .152 .428 .179 .069 .558 .452 .300 .097 .007 .139   .004 .073   88
  Control .136 .426 .165 .061 .549 .453 .294 .099 .012 .127   .005 .064   79
  Recovery .132 .412 .156 .061 .579 .456 .311 .100 .014 .119 2.002 .064   81
Note—a, upper boundary of accumulation of information over time; Ter , mean of the distribution of times taken up by the non­decision
component, in seconds. η, sz , and st represent across-trial variability in drift rate, in starting point, and in the nondecision component,
respectively. v1, v2, v3, and v4 represent the four distinct drift-rate parameters for the eight numerosity categories (see the text for
details). po , proportion of contaminants; vc , drift criterion; z, starting point of accumulation of information over time. χ2 represents
the goodness-of-fit index with critical value 102 for 76 degrees of freedom. For a total of k numerosity categories and a model with
m parameters, the degrees of freedom are k(12 2 1) 2 m, where 12 comes from the number of bins between and outside the response
time quantiles for correct and error responses for a single category (minus 1, because the total probability mass must be 1). There were
k 5 8 numerosity categories in the experiment and m 5 12 parameters in the model, so df 5 88 2 12 5 76.

1 = Sleep-Deprived, 2 = Control

1 0.6 1 1 1
2 2 2 0.20
1
0.15 2
1 1 0.5 2
1
2 2 2
2 1 0.15
0.4
0.10 0.3 0.10
0.2
0.05 0.05
0.1 Drift variability
Boundary separation a Drift rate (v1, easy) 0.00 across trials η
0.00 0.0

1
2 2 0.5 1 1
1
2 2 2 2 0.12
0.40 1 0.4 1

0.3 1 0.08 1
0.35 2
1 2 2
0.2
0.30 0.04
0.1
Start point variability
0.25 Nondecision Ter (sec) 0.0 Drift rate (v2, medium) 0.00 across trials sz

0.10 1 0.30 2 2
1 1
2 0.15
1 2
1
0.08 2 2
1
0.20 1 0.10
0.06

0.04 Contaminant 0.10 0.05

proportion po
0.02 Nondecision variability
2 2
2
1 Drift rate (v3, harder) across trials st (sec)
0.00 1 0.00 0.00

1 2 3 1 2 3 1 2 3

Session Session Session

Figure 4. Plots of the diffusion model parameters averaged over participants for the three sessions in the
experimental (sleep-deprived) group (1) and the control group (2). Sleep deprivation in Session 2 produced
significant effects of boundary separation, the proportion of contaminants, the three drift rates, starting
point variability across trials, and nondecision variability across trials. The effects on the nondecision
component and variability in drift rate across trials were not significant.
748    Ratcliff and Van Dongen

Table 2
p Values for Planned Comparisons of Parameters
Comparison of Sessions a Ter η sz v1 v2 v3 v4 po st vc z
Session 1
  Experimental vs. control .961 .997 .766 .868 .812 .411 .336 .730 .248 .970 .373 .862
Session 2
  Experimental vs. control .008* .279 .076 .000* .013* .011* .006* .255 .028* .023* .467 .021*
Session 3
  Experimental vs. control .122 .701 .016* .161 .527 .490 .948 .503 .065 .765 .728 .118
Experimental Group Only
  Sleep-deprived vs. baseline .055 .232 .118 .000* .003* .020* .012* .465 .017* .065 .429 .164
  Sleep-deprived vs. recovery .042* .392 .755 .003* .000* .002* .003* .064 .015* .004* .570 .179
Note—a, upper boundary of accumulation of information over time; Ter , mean of the distribution of times taken up by the nondecision
component, in seconds. η, sz , and st represent across-trial variability in drift rate, in starting point, and in the nondecision component, re-
spectively. v1, v2, v3, and v4 represent the four distinct drift-rate parameters for the eight numerosity categories (see the text for details). po ,
proportion of contaminants; vc , drift criterion; z, starting point of accumulation of information over time. Session 1, baseline; Session 2,
sleep-deprived (or control); Session 3, recovery. Group 3 session interactions are as follows: For a, F(2,46) 5 7.40; for Ter , F(2,46) 5
4.20; for η, F(2,46) 5 2.34; for sz , F(2,46) 5 7.04; for v1, F(2,46) 5 8.77; for v2, F(2,46) 5 10.39; for v3, F(2,46) 5 6.07; for po , F(2,46)
5 8.08; for st , F(2,46) 5 4.2. The critical value was F.95(2,46) 5 3.2.  *p , .05.

session and the baseline and recovery sessions in the ex-
perimental group, there were significant differences for
the following: boundary separation (one comparison was
marginally significant), variability in starting point across
trials, drift rates for the easier numerosity categories, pro-
portion of contaminants, and variability in the duration of
nondecision processes (one comparison was marginally
significant). Although these comparisons involved mul-
tiple t tests, the results are consistent and clear. To sum-
marize, the estimates for a, sz , v1, v2, v3, po , and st from the
sleep-deprivation session are different from the estimates
for the baseline and recovery sessions, as well as from all
of the sessions in the control group.
The differences in the parameter estimates led to the
following interpretation of the effects of sleep depriva-
tion on the two-choice numerosity discrimination task.
When deprived of sleep, most participants adopted mod-
erately more conservative decision criteria (larger bound-
ary separation), thus requiring more evidence for making
a response. However, this was not a large difference, as
compared to the effect that was seen with speed–accuracy
manipulations (Ratcliff, Thapar, & McKoon, 2001). Vari-
ability in starting point and in the nondecision compo-
nents of cognition became larger with sleep deprivation.
The former suggested that participants experienced dif-
ficulty resetting the criteria to the normal range of val-
ues observed in the nondeprivation sessions. The latter
indicated that participants were more unstable in stimulus
detection and/or more variable in executing the decision
process.
The mean of drift rates v1, v2, and v3 for the most ac-
curate numerosity categories decreased from .411 for the
baseline session to .307 for the sleep-deprivation session,
and then increased again to .438 for the recovery session.
The change induced by sleep deprivation was substantial,
suggesting that central information processing was af-
fected by sleep deprivation—specifically, the cognitive
processes that extracted an estimate of the relative nu-
merosity of the asterisk array. Sleep-deprived participants
also produced more responses that were not based on the
stimulus, but were random guesses (contaminants). How-
ever, there were large individual differences.
Individual Differences
Most of the participants in the experimental group
showed a degradation in the components of cognitive pro-
cessing from the baseline session to the sleep-deprivation
session and a rebound in the recovery session. Boundary
separation was higher in the sleep-deprivation session for 9
of 12 participants, and the proportion of contaminants was
larger for 11 of 12 participants. Most of the participants
in the sleep-deprivation group showed a decrease in drift
rate from the baseline session to the sleep-­deprivation ses-
sion and an increase to the recovery session. These results
show that the main conclusions apply to most individuals
in the study and are not the result of there having been just
a few participants showing a large effect and others show-
ing no effect. That said, systematic individual differences
in the response to sleep deprivation were observed, as has
been documented before (Van Dongen, Baynard, Maislin,
& Dinges, 2004).
Contaminant Responses
The effect of sleep deprivation on the proportion of
contaminants indicates that sleep-deprived participants
produced more responses that were not based on the stim-
ulus, but were random guesses. However, there were large
individual differences: In the sleep-deprivation session,
5 participants had under 4% contaminants, 5 had between
8% and 11% contaminants, and 2 participants had over
30% contaminants. This high estimate of the proportion
of contaminants for those 2 participants was corroborated
by accuracy values in the highest accuracy categories of
around 70% for the sleep-deprivation session and over
95% in the baseline and recovery sessions. In the baseline
and recovery sessions, none of the participants in the ex-
perimental group had over 3% contaminants. These obser-
vations are, again, consistent with previously documented
individual differences in cognitive responses to sleep dep­
rivation (Van Dongen et al., 2004).
 Sleep Deprivation Effects on Cognitive Processes     749

Number of Counts and Probability Density

150
Predicted Distribution With Predicted Distribution
Uniformly Distributed Without Contaminants
Contaminants
100

50

0
0 1,000 2,000 3,000 4,000 5,000 0 1,000 2,000 3,000 4,000 5,000

Response Time (msec) Response Time (msec)

Figure 5. Response time (RT) distributions for the participant with the most estimated contami-
nants. Five numerosity categories are grouped (see the text). The left panel shows the predicted RT
distribution with the contaminant assumption of uniform random guesses, and the right panel
shows the predicted RT distribution without the contaminant assumption, but with the same pa-
rameter values as in the left panel. The assumption of uniform random guesses produces an RT
distribution tail that adequately describes the data.

To show that the assumption of randomly distributed
contaminants is reasonable, we used the data from the
participant with the largest proportion of contaminants to
evaluate the fit of the model to the RT distribution. This
participant had similar proportions of “large” responses
across five of the numerosity categories. The average pro-
portion of “large” responses was .755, and the mean RT
was 867 msec (the five categories had proportions rang-
ing from .714 to .789 and mean RTs ranging from 794 to
875 msec); the estimated proportion of contaminants was
.38. The left panel of Figure 5 shows the data histogram
with the predicted distribution generated from the model
parameters with the contaminant assumption; the right
panel shows the predicted distribution generated from
the same model parameters but with zero contaminants.
The right panel shows that the tail of the distribution is
mispredicted; but the left panel, with the assumption of
uniform random guesses, shows the long, elevated tail that
adequately describes the data.
Discussion
In this study, the effects of sleep deprivation on distinct
cognitive processes in a two-choice decision paradigm
were investigated. Data were fit with the diffusion model,
which has previously been applied successfully in a num-
ber of other domains (see Ratcliff & McKoon, 2008). The
diffusion model accounts for both speed and accuracy of
processing in a unified approach. The model analysis of
our data showed that processes that produced evidence
from the stimulus entering the decision process were im-
paired substantially by sleep deprivation: Drift rates de-
creased by about 30% relative to baseline values. This is
a large effect, especially considering that the two-choice
task requires few, if any, perceptual or memory demands.
Thus, such a deficit in this simple two-choice task argues
for a potent effect of sleep deprivation on ability to effec-
tively extract information from stimuli.
In the sleep-deprivation condition, as compared with
the baseline condition, participants also adopted moder-
ately more conservative decision criteria, which suggests
some compensation for poorer processing in extracting in-
formation from the stimulus. Also, variability in the start-
ing point across trials was larger, and variability in the
nondecision component of processing across trials was
modestly but significantly larger. These increases suggest
a reduction in the ability to reset the decision process to
the same starting point and suggest an increase in variabil-
ity in the encoding and response-output processes.
There was a notable increase in the proportion of con-
taminants, indicating that sleep-deprived participants
made more random responses, albeit with large individual
differences. There was no trade-off across participants be-
tween the proportion of contaminants and other model
parameters; all of the other components of processing had
similar trends across participants, as a function of sleep
deprivation.
There was no increase in the duration of the nondeci-
sion component of processing, which represents the dura-
tion of stimulus-encoding and response-output processes
as a function of sleep deprivation. Also, there was no in-
crease in the variability in drift rate across trials, which
suggests that sleep deprivation simply lowers the quality
of the output from stimulus processing on all trials rather
than lowering the quality considerably on some trials but
hardly at all on other trials.
There are competing hypotheses about the underlying
mechanisms of the effects of sleep deprivation on perfor-
mance in cognitive tasks. One hypothesis suggests that
sleep loss specifically affects cognitive processes medi-
750    Ratcliff and Van Dongen
ated by the prefrontal cortex (PFC; Harrison, Horne, &
Rothwell, 2000), thereby degrading higher-order cognitive
functions, such as decision making (Harrison & Horne,
2000). Our results are consistent with this hypothesis be-
cause drift rates (central cognitive processes involved in
producing evidence from the stimulus) were reduced by
sleep deprivation. However, the effects of sleep deprivation
were not exclusively on such processes, so the hypothesis is
only partially consistent with the experimental findings.
Another hypothesis, known as the state instability hy-
pothesis (Doran, Van Dongen, & Dinges, 2001), postu-
lates that sleep deprivation induces an escalating “state
instability” that is particularly evident in experimental
tasks requiring sustained attention. This hypothesis posits
that sleep deprivation induces moment-to-moment fluctu-
ations in sustained attention due to the influence of sleep-
initiating mechanisms. Our results are consistent with
the state instability hypothesis, in that sleep deprivation
increased the number of contaminants (guesses), skewed
the RT distributions (Dinges & Kribbs, 1991) partly by in-
creasing separation of decision criteria, and increased the
across-trial variability in the starting point of the decision
process, as well as in the nondecision component. State
instability may also affect attentional networks (Posner,
2008) and, thereby, the functioning of the PFC (Durmer
& Dinges, 2005), which could explain the degradation of
stimulus processing. Although this argument needs to be
demonstrated experimentally, the state instability hypoth-
esis has the potential to provide the most comprehensive
explanation of the present findings, although the hypoth-
esized moment-to-moment fluctuations in sustained at-
tention would seem to extend to other aspects of cognition
as well. The challenge is to unambiguously link these hy-
potheses to components of processing in explicit models
so they can be subjected to experimental tests.
The nature and scope of the cognitive impairments re-
sulting from sleep deprivation have been debated for more
than a century (Doran et al., 2001; Horne, 1993; Kleit-
man, 1923; Lim & Dinges, 2008; Patrick & Gilbert, 1896;
Williams, Lubin, & Goodnow, 1959). However, progress
has been slowed by a tendency to focus on global per-
formance outcomes, with little research being done to
examine the effects of sleep deprivation on distinct cogni-
tive processes. Using the diffusion model, we were able to
study the effects of sleep deprivation on distinct cognitive
processes. Within the framework of current theories about
the effects of sleep deprivation on cognition (see Dinges
& Kribbs, 1991; Harrison & Horne, 2000), the present
results suggest that sleep deprivation degrades both atten-
tional arousal (through state instability) and central pro-
cessing. Indeed, our findings show that sleep deprivation
has wide-ranging effects on brain functioning, affecting
multiple, distinct components of cognition.
Author Note
The present research was supported by USAMRMC Award
W81XWH-05-1-0099 and DURIP Grant FA9550-06-1-0281. Prepara-
tion of this article was also supported by NIA Grant R01-AG17083 and
NIMH Grant R37-MH44640 to the first author. We thank the research
team of the Sleep and Performance Research Center at Washington State
University–Spokane and Russ Childers of the Department of Psychol-
ogy at Ohio State University for their help with the implementation of
this study. Correspondence concerning this article should be addressed
to R. Ratcliff, Department of Psychology, 1835 Neil Ave., Ohio State
University, Columbus, OH 43210 (e-mail: ratcliff.22@osu.edu).
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