Sleep, 18(5):346--354
© 1995 American Sleep Disorders Association and Sleep Research Society
Effect of Total Sleep Deprivation on Reaction Time
and Waking EEG Activity in Man
I. Lorenzo, J. Ramos, C. Arce, M. A. Guevara and M. Corsi-Cabrera
Departamento de Psicofisiologfa, Facultad de Psicologfa and Escuela Nacional Preparatoria,
Universidad Nacional Aut6noma de Mexico, Mexico
Summary: Nine paid volunteers were sleep deprived over a period of 40 hours. Every 2 hours during total sleep
deprivation (TSD) and after recovery sleep, oral temperature (OT), reaction time (RT) in a vigilance task and
electroencephalogram (EEG) with eyes open and closed (C3, C4, T3 and T4) were recorded. Ten artifact-free samples
from each condition were Fourier transformed. Absolute power was calculated for six bands. Analyses of variance
with deprivation and time of day as factors showed the following significant results: 1) TSD induced an increase
in RT, of theta power in all derivations, of beta power in both centrals and a decrease of alpha power with eyes
closed; OT was not affected. 2) All bands showed a peak of power at 1800 hours, 2 hours in advance of the OT
acrophase at 2000 hours. All variables recovered baseline values after 1 night of sleep. Significant linear correlations
of hours of wakefulness with EEG and R T, and of EEG power with OT and R T, were observed. The present findings
show a linear increase in EEG power and RT with TSD, and a diurnal oscillation ofEEG power, which is independent
of TSD. Key Words: EEG power-Oral temperature-Reaction time-Sleep deprivation.
We have previously demonstrated in two independent studies in men (1,2) and one in rats (3) that waking
electroencephalogram (EEG) activity is modified depending on the amount of previous sleep or wakefulness. After a normal period of wakefulness (16 hours),
EEG power is significantly increased and interhemispheric correlation is decreased. After a normal night
of sleep, morning values are recovered. Extended hours
of wakefulness, for example 1 night of sleep deprivation, exacerbate the EEG changes, which are reversed
by 1 night of recovery sleep. The changes in the waking
EEG are dependent on the amount of previous sleep
or wakefulness and are independent of the time of day,
because EEG power decreases and interhemispheric
correlation increases after both diurnal and nocturnal
sleep (2).
These findings indicate that the need for sleep, built
up by accumulating hours of wakefulness, is reflected
not only in the sleeping EEG, as demonstrated by other
studies (4-6), but also in the waking EEG.
The aim of the present study was 1) to corroborate
once more the effect of prolonged wakefulness on the
waking EEG; 2) to investigate the time course of EEG
Accepted for publication February 1995.
Address correspondence and reprint requests to L Lorenzo, Departamento de Psicofisiologia, Facultad de Psicologia, Escuela Nacional Preparatoria, Universidad Nacional Aut6noma de Mexico,
Mexico, D.F. 04510, Mexico.
changes by recording brain activity every 2 hours over
a period of 40 hours of continuous wakefulness; 3) to
investigate the relation between EEG changes and performance in a vigilance task; 4) to explore the relationship of these changes to other physiological parameters, in this case oral temperature and 5) to explore
the recovering effect of different numbers of hours of
sleep.
With these purposes in mind, EEG activity during
rest with eyes open and closed, oral temperature (OT)
and reaction time (RT) in a vigilance task were recorded every 2 hours during 40 hours of sleep deprivation. Because evidence from other studies has shown
that the EEG is different in men and women (7-12),
only men were included in this study.
Although coherence and correlation analyses are frequently considered to be equivalent and to provide
similar information, the former in frequency domain
and the latter in time domain, we preferred correlation
over coherence because it is independent of voltage,
whereas coherence is influenced by power (13; Guevara
and Corsi-Cabrera, unpublished).
METHODS
Subjects were recruited from an announcement
within the University community soliciting paid volunteers to participate in the study.
346
347
WAKING EEG DURING TOTAL SLEEP DEPRIVATION
TABLE 1. Mean of absolute power in square microvolts before (Pre) and after (Post) total sleep deprivation and percentage
of change (100% = Pre)
T4
T3
C4
C3
Pre
Post
%
Pre
Post
%
Pre
Post
%
Pre
Post
%
Delta
Theta
Alpha I
Alpha2
Betal
Beta2
18.15
12.82
5.55
6.48
4.78
4.54
23.38
17.61
6.46
7.75
6.05
5.46
28*
37*
16
19
26*
20*
19.01
13.07
6.03
6.98
5.08
4.90
20.82
16.10
6.37
7.79
5.72
5.69
Eyes open
9
23*
5
11
12
16
9.30
5.55
2.46
2.70
3.16
3.89
11.56
6.85
2.54
2.98
3.15
3.56
24*
23*
3
10
-1
-9
9.60
5.40
2.51
2.82
3.11
4.08
9.43
6.21
2.52
3.09
3.44
4.49
-8
15
Delta
Theta
Alpha 1
Alpha2
Beta 1
Beta2
19.82
16.11
15.16
15.62
7.62
6.70
25.05
21.62
12.80
15.04
8.98
7.10
26*
34*
-16
-4
17
5
20.45
17.37
16.10
16.62
7.82
6.52
22.94
20.30
12.46
15.37
8.44
6.84
Eyes closed
12
16*
-23*
-8
7
4
10.17
6.66
5.45
5.20
4.06
3.75
11.33
7.82
4.33
4.76
3.82
3.03
12
17
-21*
-9
-6
-20
10.50
6.84
5.69
5.84
3.67
3.46
10.32
7.39
4.42
5.08
3.77
3.29
-2
8
-23*
-14
2
-5
9
10
10
The main effect of deprivation is shown and the time of day is pooled (ANOYA: deprivation by time of day: 0800, 1000, 1200, 1400,
1600, 1800 and 2000 hours).
* p < 0.009.
Potential subjects underwent a careful interview and
filled out questionnaires on sleep habits and health.
Only right-handed subjects (14) showing normal sleep
habits (bedtime between 2300 and 2400 hours), free
from sleep alterations and without central nervous system disorders or use of drugs known to affect the EEG,
were included. The final sample was comprised of 10
male students from 22 to 30 years old.
Subjects slept 2 nights in the laboratory, the first for
habituation to the recording procedures and the second
as control. After spontaneous awakening, between 7
and 8 a.m., subjects remained awake for 40 hours (±30
minutes, until 2400 hours of the next day) under continuoussurveillance in the laboratory. They were required to refrain from alcohol and caffeine intake during the study. Thereafter, I night of recovery, beginning
at 2400 hours and divided into three blocks of sleep,
was allowed (R I, R2 and R3): subjects were awakened
after two full sleep cycles or after 3 hours of sleep,
whichever occurred first. This difference in time arose
because subjects in paradoxical sleep were not awakened until it spontaneously finished. During sleep deprivation, EEG, oral temperature (OT) and reaction
time (RT) in a vigilance task were recorded every 2
hours, and 10 minutes after awakening from R I, R2
and R3.
The vigilance task lasted I 5 minutes. One hundred
fifty visual stimuli were displayed, one at a time, for
SO milliseconds on a video screen. The intertrial interval ranged randomly from 5 to 7 seconds. Stimuli
consisted of four white squares, each one missing one
of the corners (3.7 x 3.3 cm), presented in a random
sequence. Preceding the task, one of the four patterns
was selected and the subject was asked to press the
"enter" button on the keyboard as soon as possible
each time the selected pattern appeared. Reaction time,
omissions and errors were computed.
Sleep was recorded, and sleep architecture was analyzed according to standard procedures (IS). EEG was
recorded using a Grass model 8-16E polygraph with
filter setting at 1 and 35 Hz with electrodes attached
according to the 10-20 International System at C3, C4,
T3 and T4 referred to ipsilateral earlobes. Impedance
was kept below 10 kilohms. These derivations were
chosen because changes observed in previous studies
at central derivations are similar to those observed at
parietal and occipital derivations, whereas the temporal cortex often showed a different pattern (1,2,8).
Ten artifact-free epochs of2 seconds each were captured every 2 hours during wakefulness with eyes open
and closed, and after R I, R2 and R3 in a personal
computer through an analog--digital converter, 12-bit
resolution, at a sampling rate of 128 Hz. Criteria for
selecting epochs for spectral analysis included a compromise between stationarity and stability ofEEG between successive epochs; 10 2-second samples met both
criteria and provided enough resolution for waves between 0.5 and 64 Hz without compromising stability
(16). Much attention was paid to avoid epochs showing
signs of sleepiness or stage I sleep. EEG epochs were
Fast Fourier transformed using a square window, and
absolute power (AP) was obtained for the following
bands: delta (1.5-3.5 Hz), theta (4-7.5), alphal (7.59.5), alpha2 (10-12.5), beta I (13-17.5) and beta2 (1825.5). For statistical purposes, AP was log transformed
(17).
The following statistical analyses were used: oneand two-way analyses of variance (ANOVAs) for reSleep, Vol. 18, No.5, 1995
I. LORENZO ET AL.
348
log (micV')
log (micV2)
.·····PRE
3.5
_POST
3.0
3.0
2.8
2.5
2.0 _
1.5 -
2.4
1.0L--•.,...---.r-.----r---'!""""--~.,r.--"""'T-delta
theta
alpha!
alpha2
beta,
2.2
beta2
,
i
1~
i
,
'2~
i
I
24
,
~2
I
,
,
4'0 TSDCh)
24
16
CT
C4: p < 0.003) and closed (C3: p < 0.001; C4: p <
0.007), and at T3 with eyes open (p < 0.004); 2) for
delta AP at C3 (p < 0.001) and T3 (p < 0.002) with
eyes open, and at C3 (p < 0.001) with eyes closed and
3) for beta1 (p < 0.001) and beta2 (p < 0.005) at C3
with eyes open. Alphal AP decreased significantly
(23%) at C4, T4 (p < 0.002) and T3 (p < 0.007). The
theta band, the central cortex and the left hemisphere
with eyes open showed more significant changes with
sleep deprivation than the temporal cortex and the
right side.
To assess the time course of power rise during TSD,
Pearson product-moment coefficients were calculated
between the 21 EEG measurements and hours of wakefulness. Changes in theta AP with TSD correlated positively (p < 0.01) with accumulating hours of wakefulness at all derivations with eyes open (r = C3: 0.74;
C4: 0.69; T3: 0.72; T4: 0.54) and at C3 (r = 0.71) and
T3 (r = 0.58) with eyes closed (Fig. 2). Significant
positive correlations were also observed at C3 for delta
(r = 0.59), beta1 (r = 0.70) and beta2 (r = 0.60) with
eyes open and, for delta (r = 0.72) and beta 1 (r = 0.53)
with eyes closed. Delta AP at T3 with eyes open also
showed a positive correlation (r = 0.65). On the other
hand, alphal AP at T3 with eyes closed correlated
negatively with hours of TSD (r = -0.53).
There was a significant overall effect oftime-of-day,
mainly for the fast frequencies, alpha2, beta 1 and beta2:
RESULTS
Absolute power (AP)
To explore the effect of sleep deprivation and time
of day on waking EEG, the EEG of the control day
(PRE-D) was compared to the EEG of the post-deprivation day (POST-D). Only results from 0800 to 2400
hours were considered for these analyses because there
was no equivalent control for results from 0200 to 0600
hours. Two-way ANOVAs for repeated measures with
deprivation (df= 1,136) and time of day (df= 8,136)
as factors were used separately for each derivation and
band, with the significance level set at p < 0.009 to
reduce type I error.
In general, total sleep deprivation (TSD) induced a
global increase in AP of all bands with eyes open and
closed, except for alphal and alpha2 AP with eyes
closed, which decreased from PRE-D to POST-D (Table 1). The maximum increase reached 37% and 34%
for theta at C3 with eyes open and closed, respectively.
The increase in power POST -D was significant for the
following bands and derivations: 1) for theta AP at
both centrals with eyes open (Fig. 1) (C3: p < 0.001;
Time of day showing minimum (Min) and maximum (Max) values of EEG absolute power with eyes open and
percentage of change (% = MaxiMin)
C3
Delta
Theta
Alpha 1
Alpha2
Beta 1
Beta2
,
FIG. 2. Linear trend between 40 hours of sleep deprivation (TSD)
and theta absolute power, log transformed, every 2 hours at C3 with
eyes open. Clock time (CT) is also indicated.
peated measures and Tukey's Student t tests for pairwise comparisons, Pearson product moment correlation and crosscorrelation function.
Bands
,
16
FIG. 1. Mean and standard error of absolute power, log transformed, for six bands at C3 with eyes open during the control day
before deprivation (PRE) and during the day of deprivation (POST).
The main effect of deprivation with time of day pooled is shown
(ANOVA: deprivation x time of day). *p < 0.009; **p < 0.001.
TABLE 2.
,
Min
0800
0800
0800
Max
1800
1800
1800
* P < 0.009.
Sleep. Vol. 18. No.5. 1995
C4
%
35*
33*
48*
Min
0800
0800
0800
0800
Max
1800
1600
1800
1800
T4
T3
%
19*
22*
34*
47*
Min
0800
1000
1000
Max
1800
1800
1800
%
32*
34*
49*
Min
Max
%
1200
1200
1800
1800
22*
31*
1200
1200
1200
1800
1800
1800
36*
32*
42*
349
WAKING EEG DURING TOTAL SLEEP DEPRIVATION
A
2.2
2.0
1.8
1.6
L-~------P-----~----~~----T-----~------~----~----~----
*--------------------------*
*---------------------------------*
CLOCK TIME
B
1. 8
-
1.6 -
1.4
1.2 -
1.0L-~------~----~----~----~------~----~1------~----~1--h
8
12
16
20
24
*-------------------------*
*---------------------------------*
*----------------------------------------------------*
CLOCK TIME
FIG. 3. Mean and standard error of absolute power, log transformed, of alpha2 (A) and beta2 (B) at C3 with eyes open every 2 hours
from 0800 to 2400 hours. The main effect of time of day with days pooled is shown (ANOYA: days x time of day). Connecting lines at
the bottom of the figure indicate significant differences between means. (Tukey's Student's t test for pairwise comparisons p < 0.05.)
Sleep, Vol. 18, No.5, 1995
I. LORENZO ET AL.
350
A
2.0
1 .8
1.6
1.4
~----~----------_r----------~------------~----------_r----
*-----*------------------*
B
msec
240
220
200
180
160
140~____~___________r----------~~--------~~----------~-----
o
40
R1
*-----*
* -----------*
R2
R'3
* -----------------*
FIG. 4. Recovery. Mean and standard error of absolute power, log transformed, of theta at C3 with eyes open (A) and reaction time (B)
in milliseconds during the performance of a vigilance task at 0800 hours of the control day (0), after 40 hours of sleep deprivation (40)
and after one (R l), two (R2) and three (R3) blocks of recovery sleep, 3 hours each. Connecting lines at the bottom of the figure indicate
significant differences between means. (Tukey's Student's t test for pairwise comparisons p < 0.05.)
for alpha2 at C3, C4 and T4 (p < 0.009), for beta1 at and for alpha1 at C4 (p < 0.003). With eyes closed it
C4, T3 and T4 (p < 0.003) and for beta2 at the four was significant only for beta2 at C3 and T3, and for
derivations (p < 0.001). The time-of-day effect was alpha2 at T4 (p < 0.001). However, the same nonsigalso significant for delta and theta at T4 (p < 0.001) nificant trend could be observed for the rest of the
Sleep. Vol. 18. No.5. 1995
WAKING EEG DURING TOTAL SLEEP DEPRIVATION
260
351
msec
= 49.81; p < 0.00 I]. Deprivation and interaction were
not significant. OT was significantly lower at 0600,
0800 and 1000 hours compared to the maximum value
attained at 2000 hours.
Hours of continuous wakefulness and OT were not
correlated. However, OT was significantly correlated
140
to AP of fast frequencies: alphal at C3 (r = 0.55) and
T3 (r = 0.54) and betal at T4 (r = 0.78) with eyes
120 T'T""",......,r-r"""'T"-,-"""".,.....r-;,---r,-;-,I,""""T,"""'T"....,....-r--r-~
o
16
24
32
40 TSO(h)
open; and alpha2 and beta2 at all derivations, and
16
24
16
24 CT
betal at both temporals with eyes closed (alpha2: C3
FIG. 5. .Line~r trend between 40 hours of sleep deprivation (TSD)
and reactIOn tIl!I~ every 2 hours, in milliseconds, during the perfor= 0.73; C4 = 0.65; T3 = 0.62; T4 = 0.58; beta2: C3
mance of the vigIlance task. Clock time (CT) is also indicated.
= 0.60; C4 = 0.59; T3 = 0.62; T4 = 0.58; betal T3 =
0.53; T4 = 0.58).
Because OT and AP showed significant time-of-day
derivations and bands. There were no significant deeffects, crosscorrelations were calculated between them.
privation by time-of-day interactions.
Pairwise comparisons (Table 2) showed a peak of Correlation values increased when OT was advanced
power at 1800 hours compared to the lowest value 2 hours and became significant for AP of all bands and
which was always before noon. The maximum peak derivations except for beta I at T3 with eyes open, and
was observed at 1800 hours for all bands and deri- for alphal at C4, T3 and T4, for betal at C4 and T3
vations except for alpha2 at C4 with eyes open and at and for delta at T4 with eyes closed.
T4 with eyes closed. This band showed higher power
at 1600 and 1800 hours. Beta2 also showed a signifi- Vigilance task
cant peak of power at 2400 hours. The minimum power was observed at 0800 hours for all bands at C3 and Reaction time (RT)
C4, at 1000 hours for betal and beta2 at T3 and at
The two-way ANOYA showed a significant main
1200 hours for all bands at T4 (Fig. 3).
effect
for deprivation [F(1, 144) = 49.81; p < 0.001]
Two-way ANOVAs were performed on AP with recovery (0800, 2400, RI, R2 and R3; df = 4, 72) and with RT higher on the POST-D day. Although a nonhemisphere (df = I, 72) as factors. There were no hemi- significant increase of R T at 0600 hours could be obsphere effects nor interactions. The recovery main ef- served, there was no significant time-of-day effect, nor
fect was significant for the following bands: theta at interaction. There was also a positive correlation (r =
central derivations with eyes open (p < 0.007) and 0.85) between hours of wakefulness and reaction time
closed (p < 0.005), and at temporals with eyes closed (Fig. 5), and between thetaAP at C3 and RT (r= 0.53).
(p < 0.003); delta at centrals with eyes closed (p < Omissions and errors were pooled every 6 hours. The
0.002); betal and beta2 at temporals with eyes open Friedman test showed significant differences for
(p < 0.001) and at centrals and temporals with eyes omissions (Xr = 23.5; p < 0.0006). The Wilcoxon test
closed (p < 0.001). Pairwise comparisons showed sim- showed that the number of omissions increased sigilar results with eyes open and closed: the main effects nificantly during 0200 to 0600 hours compared to the
of deprivation described above were confirmed and previous day, and that they continued to increase duralthough theta, beta I and beta2 power remained higher ing 1400 to 1800 and 2000 to 2400 hours of the dethan baseline values after RI, the difference was no privation day, compared to the control day, as well as
longer significant and, after R2 and R3, the level of to 0200 to 0600 hours. Although the number of errors
AP was similar to baseline values and significantly also increased it did not reach significance levels.
The one-way ANOYA on recovery values ofRT was
lower than after 40 hours of sleep deprivation (Fig.
4A). Delta power at central derivations showed a fur- significant [F(4, 32) = 7.0; p < 0.001]. Pairwise comther significant increase after R I and recovered base- parisons showed that R T remained higher than baseline values after R2. Beta power at temporal deriva- line after RI and R2 and recovered baseline values
tions showed a negative rebound; in R2 it decreased only after R3 (Fig. 4B).
to lower than baseline values and it returned to PRE-D
values after R3.
Sleep stages
240
Oral temperature (OT)
Sleep stages (Table 3)
The two-way ANOVA (deprivation by time of day)
only showed a significant time-of-day effect [F(I, 144)
Statistical analysis of the main sleep variables between control and recovery night (StUdent's t tests)
Sleep, Vol. 18, No.5, 1995
I. LORENZO ET AL.
352
TABLE 3. Sleep stage parameters for control and recovery night after sleep deprivation divided in three blocks of 3 hours
each (RI, R2 and R3)
Control
RI
430*
Total sleep time (minutes)
195
0.92*
0.96
Sleep efficiency index
7.50*
4.21 **
Time awake %
7.64
6.20
Stage I %
51.5
47.30
Stage 2 %
15.00
22.02**
Stage 3+4 %
Paradoxical sleep %
25.71
25.12
Latency to stage I (minutes)
6.75*
2.57
11.07*
3.92
Latency to stage 2 (minutes)
Differences between control and R 1 + R2 + R3; one-way ANOVA, * P < 0.02.
Differences between RI, R2 and R3: Student's t tests, ** p < 0.01.
showed the following significant results: the average
time of sleep and the sleep efficiency index were significantly higher, whereas the average time in wakefulness, and latency to stage 1 and 2 sleep, were significantly lower during the recovery night. The amounts
of time spent in stage 1 and 2 sleep were slightly different but they did not reach the significance level,
probably due to intersubject variability. The comparison between Rl, R2 and R3 (one-way ANOVAs)
showed significant differences only for stage 3 + 4 sleep,
and for average time in wakefulness, both of which
were higher during R 1.
DISCUSSION
The effect of sleep deprivation
Sleep deprivation resulted in: 1) A deterioration in
performance of the vigilance task; 2) a linear increase
of power that was more prominent on the theta band,
on central than on temporal derivations and on the
left than on the right side with eyes open and 3) a
decrease of alphal AP with eyes closed. In addition
we found a diurnal peak of power at 1800 hours evident
PRE-D as well as POST-D. The lack of interaction
between TSD and time-of-day points toward orthogonal influences of both processes on EEG power.
The EEG results clearly demonstrate that TSD is
reflected on the waking'EEG and corroborate previous
findings (1,2). However, in the present experiment the
effects were restricted to some bands and derivations.
These discrepancies can be attributed to several factors: first, to the duration of TSD (24 hours in the
mentioned studies and 40 hours in the present experiment); second, to the frequency of EEG evaluations
(in the above-mentioned studies, results were based on
one morning and one night recording only, whereas in
the present report, results are based on evaluations
every 2 hours) and third, the characteristics of the subjects participating in each study. Previous studies included men and women, whereas in this report only
Sleep, Vol. 18, No.5, 1995
R2
R3
RI+R2+R3
186
0.98
1.92
4.07
48.00
13.57
34.42
1.00
3.92
160
0.94
2.23
4.92
49.85
11.71
33.42
1.14
4.50
541
0.96
3.29
5.06
48.38
15.76
30.98
1.57
4.11
men participated. Several studies have reported important EEG differences between men and women (812). Perhaps EEG activity is affected to a greater extent
by TSD in women than in men. However, this hypothesis needs to be tested.
The present results also agree with other studies in
which higher theta and alpha are reported in association with failures in performance during daybreak in
night workers (I8-20), and with longer reaction time
to acoustic stimuli (21). The decrease of slow alpha
frequencies with TSD during the eyes closed condition
is also consistent with the reduction reported for this
band in other studies (22-24).
However, we also observed an increase ofbetal and
beta2 power. Although beta can be considered as an
index of arousal (25), it has been reported to be higher
during rest in subjects with lower scores in intelligence
and aptitude tests than in subjects with higher scores
(Arce et aI., in preparation), and during the premenstrual phase when performance decreases (26). These,
together with the fact that it increased simultaneously
to theta AP and to RT, suggest the result of an effort
to maintain wakefulness.
Reaction time in the vigilance task was longer
POST-D than PRE-D, as expected according to the
literature (27-29), and this cannot be attributed to a
decline in the subject's concern to detect signals because a similar number of errors was maintained along
TSD (30).
The time course of changes induced by TSD showed
a linear increase with accumulating hours of wakefulness, negative for alpha power with eyes closed and
positive for RT and for the rise in theta power, as well
as for the other bands. The deterioration of RT with
TSD was positively correlated to theta AP at C3 with
eyes open; performance got poorer as theta AP increased. These results indicate a relation between cortical theta activity and performance.
On the other hand, OT was not affected by TSD.
Studies in rats have demonstrated that prolonged TSD
induces a dramatic decrease in body temperature, how-
WAKING EEG DURING TOTAL SLEEP DEPRIVATION
ever this effect is observed preceding the death of the
animal after 10 or 32 days ofTSD (31). Contradictory
results have been reported for men (27), but the present
findings show that 40 hours of TSD are not enough to
induce changes in their oral temperature.
An interesting and surprising effect not previously
described was the presence of a diurnal peak of power
at 1800 hours for most bands and at 1600 hours for
alpha evident PRE-D as well as POST-D. According
to circadian literature, significant changes in EEG power could more probably be expected in association with
the wakefulness maintenance zone at 2000 to 2200
hours, or with sleep propensity at 1400 hours (32-34).
The acrophase of OT was found to be at 2000 hours
and the trough at 0600, 0800 and 1000 hours as described in the literature (35), in spite of different meal
and labor schedules in Mexico City (main meal between 14 and 15 hours). However, both phenomena
may be related because OT showed positive correlations with EEG power, mainly for high frequencies,
and crosscorrelation analysis showed that the EEG
acrophase was 2 hours in advance ofthe OT acrophase,
whereas the trough of both curves was in phase at 0
lag.
All EEG parameters recovered baseline values after
the first block of sleep except for delta. Reaction time
and omissions required the three blocks of sleep to
recover baseline values. Delta power and RT continued to increase after R 1 to higher levels than after 40
hours of deprivation. Although much attention was
paid to avoid EEG segments showing signs of sleepiness, the increase of delta power and RT together suggest that subjects were not fully alert. In fact, it was
very difficult to awaken them and lead them to the next
room for task performance.
The beta band at temporal derivations (beta2 with
eyes open and beta 1 and beta2 with eyes closed) showed
a negative rebound. Friedman et al. (36) also observed
a negative rebound of delta waves during sleep in the
rat and advanced two possible explanations for this
phenomenon: one, that it was a consequence of the
activation ofa sleep inhibitory mechanism that would
suppress sleep under normal conditions and would be
hyperactivated after sleep deprivation; and, two, that
it was an oscillatory response of a servomechanism.
Although it is not possible to know if the EEG changes
observed in the present experiment reflect the need for
sleep, built up by accumulating hours of wakefulness,
or if they are a consequence of the lack of sleep, in the
same way as hunger and inanition do not induce the
same symptoms (37), the present findings show that
with TSD there is a linear increase of EEG power during wakefulness, mainly of theta and beta bands, parallel to the deterioration in performance, that is independent of the time of day, and that there is a diurnal
353
oscillation of EEG power with a peak 2-4 hours in
advance of the OT acrophase independent of the
amount of prior sleep or wakefulness.
Acknowledgements: Isabel Perez-Monfort corrected the
English version of the manuscript. This work has been partially financed by CONACYT 0663-H9111.
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