Effect of Morning and Afternoon Naps on Mood After

Effect of Morning and Afternoon Naps on Mood
After Total Sleep Deprivation in Patients
with Major Depression
Michael Wiegand,* Dieter Riemann, Wolfgang Schreiber,
Christoph J. Lauer, and Mathias Berger"
In 30 depressed patients who had responded to total sleep deprivation therapy, morning naps
led more frequently to relapses into depression than did afternoon naps. Longer naps were
less detrimental than shorter ones, and there was no significant relationship between the effect
of a nap on mood and its content of slow-wave-sleep. The amount of the rapid eye-movement
sleep, too, was unrelated to clinical nap effects. Thus, some of the current theories on the
re!ati~nsh;.p between sleep and depressive symptomatology are not supported by the data.
Our results demonstrate the importance of nap timing, suggesting a circadian variation of
propensiC¢ to relapae into depression.
Key Words: depression, total sleep deprivation, naps
Total sleep deprivation (TSD) is an effective treatment for
major depression (for review, see Gerner et al 1979; Gillin
1983; Wu and Bunney 1990). According to Wu and Bunney, who reviewed 61 articles on the topic, including over
1700 individual patients, the overall response rate reported
in the literature is 59%. In contrast to other antidepressant
treatments, the therapeutic effect develops rapidly, but a
relapse into depression usually occurs after the following
nocturnal sleep; 83% of patients not receiving medication
and 59% of patients receiving medication are reported to
relapse after the first night of sleep (Wu and Bunney 1990).
From the Max Planck Institute of Psychiatry, (MW, WS, CJL) Munich, and Central
Institute of Mental Health (DR, MB), Mannheim, Germany.
Address reprint requests to M. Wicgand, M.D., Psychia_nicClinic of the Technical
University of Munich, Ismaninger Strasse 22, W-8000 Miinchen 80, Germany.
*Current address: Psychiatric Clinic, Technical University of Munich, Germany.
tCurrent address: Psychiatric Clinic, University of Freiburg, Germany.
Received March ! 1, 1992; December 4, 1992.
© 1993 Society of Biological Psychiatry
Although limited in its clinical usefulness, TSD has
become an important paradigm in research on affective
disorders. To elucidate its mechanism of action, previous
sPddies have tamed to identify predictors of response to
TSD (Gillin 1983; Roy-Byrne et al 1984). Accordiag to
Duncan et al (1980), response to TSD is predicted by a
baseline sleep electroencephalographic (EEG) pattern with
features typical for depression [increased intermittent and
early morning awakening, reduced rapid eye-movement
(REM) latency, reduced sleep efficiency]. In a study with
a larger sample, Riemann et al (1991) confirmed the predictive value of a shortened REM latency for response to
TSD. Other reliable neurobiological predictors, especially
neurochemical ones, have not yet been identified. Among
clinical va_dables, diurnal variation in mood is clearly related to response to sleep deprivation (Reinink et al 1990;
Riemann et al 1991).
In the present study, an alternative experimental approach to investigate the antidepressant properties of sleep
M. Wiegand et al
deprivation is presented. It is based on clinical observations that point to the reversibility of a favorable sleep
deprivation effect by a short daytime nap. In an early report
by Pflug and T611e (1971), it was mentioned for the first
time that in some responders to TSD, a daytime nap after
successful sleep deprivation provoked a worsening of mood.
In a single case study, Knowles et al ~¢I OTO~,,.,described_ a
relapse into depression caused by a short nap (15 min of
non-REM sleep) in the early morning (5:00 AM), and RoyByrne et al (1984) observed a severe mood worsening
subsequent to as little as 90 sec of polysomnographically
recorded sleep at 3:30 PM. In a single case study of 48-hr
sleep deprivation, Southmayd et al (1987) observed a relapse in a TSD responder after several very short episodes
of sleep during the second deprivation night, with a cumulated total of 11.1 min of stage 2 sleep, revealed by
continuous EEG monitoring.
The observations from these anecdotal re~ tn~ts and case
studies could be confirmed by some systematic investigations. In the first study on this topic (Wiegand et al
1987b), we observed effects ranging from improvement
to dramatic worsening in drug-free depressed patients who,
after TSD, took a nap at 1:00 PM. In 6 of 12 responders
to TSD, the nap led to a clear relapse into depression. The
results of this pilot study did not allow definite conclusions
as to the respective determinants of relapse but pointed to
the role of longer nap sleep duration and the occurrence
of REM sleep as crucial factors. In a separate analysis of
hourly mood r,:tings before and after the naps, we found
a delayed mooa setback in those TSD responders who had
not worsened immediately after the nap (Wiegand et al
Other systematic studies yielded inconsistent results.
Kraft et al (1984) described a relapse in one of seven
depressed patients after a 10-min afternoon nap following
response to sleep deprivation. Gillin et al (1989), however,
did not observe such relapses following 10-min naps at
8:30 A M or 3:00 r,M In a ~ h l d v i n n a t i ~ n t e r,~t,,~i,,in,-, ,-~,~d
ication, Giedke (1988) observed no consistent effect of
naps at 1:30 PM on mood. Wu and Bunney (1990) ment;oned unpublished data from their group showing relapses
in five of seven TSD responders after a 60-min nap.
The antidepressant effect of sleep deprivation and its
v y oa~,,,,l.~ ~ u a y u i u ~ , ii&pS as w r i i d~ liOi.,tl.tilldl
supports the hypothesis that sleep can be depressiogenic
in depression. This assumption is further supported by the
frequent clinical phenomenon of positive diurnal variation
in mood, with a maximal depressed mood in the morning
and a gradual improvement during the course of the day
(Haug and F/ihndrich 1990).
Several hypotheses have been proposed to explain the
antidepressant eur.t:t
".... of sleep deprivation and, conversely,
the "depressiogenic" properties of sleep in depression.
Among these, the following are presently the most dis-
cussed (van der Hoofdakker and Beersma 1988; Wu and
Bunney 1990):
1. Several theories emphasize the involvement of circadian processes in these phenomena. Under a chronobiological perspective, major depression can be characterized by an alteration of the "internal clock". Sleep
deprivatioa is presumed to exert its antidepressant action
by either resynchronizing disturbed rhythms or by preventing sleep during a so-called critical phase in the early
morning hours (Wehr and Wirz-Justice 1981; Kripke 1984).
In light of these theories, the timing of a daytime nap
following sleep deprivation can be expected to be crucial
to its effect on mood and depressive symptomatology.
2. The "two-process model" of sleep (Borb61y, 1987;
Borb61y and Wirz-Justice, 1982) postulates a deficiency
in a homeostatic "process S" (associated with EEG slowwave activity) in depression that may account for the im'~irm,~nt in mood. Sleep depfivatien is pi~umed to increase the level of"process S" by lengthening the duration
of wakefulness, thus leading to improvement in mood.
This model allows the prediction that the depressiogenic
impact of sleep is related to the degree of "process S"
reduction. Correspondingly, the EEG slow-wave activity
during a nap can be expected to be essential to its "depressiogenic" action.
3. Wu and Bunney (1990) proposed the hypothesis of
a sleep-associated depressiogenic process, possibly represented by a substance that is released during sleep and
is metabolized during wakefulness. In many respects, this
theory resembles the Borb61y and Wirz-Justice model; the
latter differs from the former in implying a "euphorogenic"
substance released in wakefulness rather than a "depressiogenic" substance released during sleep. Both theories
allow the hypothesis that longer naps are more detrimental
than shorter ones and that longer prior wakefulness protects
against the mood worsening caused by daytime naps.
4. With regard to the antidepressant effect of selective
REM sleep deprivation observed by Vogel et al (1980), it
has been hypothesized that REM sleep suppression is essential to the beneficial effects of several antidepressant
treatment modalities, including sleep deprivation (Berger
et al 1990). This view is in line with the cholinergicadrenergic imbalance model of depression (Janowsky et
al 19';-'2)and the reciprocal interaction model of REM sleep
regulation (McCarley ! 982). In light of this approach, the
occurrence of REM sleep during a daytime nap, as a correlate of elevated cholinergic neuronal activity, should be
accompanied by a greater propensity of relapse into depression.
The induction of depressive symptomatology by short
sleep episodes can be regarded as a cmcia! experiment to
test these hypotheses. The study presented here was designed to examine this phenomenon systematically to elu-
Naps After Sleep Deprivation in Depression
cidate the nature of the depressiogenic properties of sleep
in depression. The main purpose was to examine the relationship between the clinical effects of daytime naps
following sleep deprivation and the timing of the nap
(morning versus afternoon). Other factors were also considered: the length of a nap as well as the occurrence and
the amount of both slow-wave sleep and REM sleep. Special emphasis was placed on the possible interaction of
these variables with nap timing.
The study was performed simultaneously at the Max Planck
Institute of Psychiatry, Munich, and the Central Institute
of Mental Health, Mannheim, Germany (part of the data
have been published previously by Wiegand et al 1989).
Thirty inpatients [10 male, 20 female, 9 single episode,
21 recurrent episodes; mean age 48.7 ___ 11.5 (SD) years]
suffering from a major depression according to DSM-IIIR (296.2 x , 296.3 x , 296.5 x , rated by experienced psychiatrist), with a mean baseline depression score ( _ SD)
on the Hamilton Depression Rating Scale, 2 l-item version
(HAMD-21) of 26.9 +__ 5.3 (minimum 18 points) were
included in the study. Informed, written consent was obtained from all patients.
After a drug washout period of at least 7 days and an
adaptation night in the sleep laboratory, followed by one
night of polysomnography, patients were subjected to a
TSD. On the following day, patients took a nap in the
sleep laboratory (with polysomnographic recording) either
at 9:00 AM or 3:00 PM, they were assigned randomly to
the morning versus afternoon nap condition. Sleep recordings were terminated when the patient woke up spontaneously without falling asleep again within 5 min.
In the morning nap group, two patients did not fall
asleep at the scheduled nap ume and were excluded from
the present analysis. Gender ratio, mean age, and baseline
psychopathology of the resuhmg sample are characterized
in Table 1. With regard to these variables, there were no
significant differences between the morning and afternoon
nap groups nor between responders and nonresponders to
The recordings were performed using a 17-channel Nihon
Kohden 4417 EEG machine that measured the following
parameters: EEG (C3-A2/C4-AI), electro-ocuaog~am ~norizontai), and electromyogram (submental). The sleep polygraphs were rated visually according to standard criteria
(Rechtschaffen and Kales 1968). The following definitions
of sleep parameters were used:
1. Total sleep time: time spent asleep less any awake
2. Sleep onset latency: time from lights out until the
appearance of stage 2 sleep.
3. Sleep efficiency: ratio of total sleep time to time in
4. REM latency: time from sleep onset until the first
occurrence of REM sleep.
5. REM density: number of 3-sec "miniepochs" of REM
sleep containing eye movements as a percentage of
the total number of "miniepochs" of REM sleep.
Depression Ratings
Depressive symptomatology was observer rated by means
of the six-item version of the Hamilton Depression Scale
(HAMD-6) (Bech et al 1975) covering depressed mood,
guilt feelings, woik and haterest, psychomotor retardation,
anxiety (psychic), and physical symptoms (maximum score
22); ratings took place on the day before TSD at approximately 9:00 AM and 3:00 PM and on the day following
TSD approximately 9:00 AM and 11:00 AM (or 30 min
after termination of a morning nap, respectively) and 3:00
PM and 5:00 PM (or 30 min after termination of an afternoon
nap, respectively). Raters were unaware of the experimental conditions. Response to total sle~:p deprivation was
defined as a reduction of at least 30% in the HAMD-6
score, based on both 9:00 AM ratings. A nap effect (difference in HAMD-6 ratings after versus before the nap)
of four points or more was defined as a relapse; changes
between one and three points were termed a slight worsening. The difference in HAMD-6 ratings between 9:00
AM and 3:00 PM on the day before TSD is referred to as
morning/afternoon variation of mood.
Statistical Analyses
Comparisons between subgroups were mainly performed
by means of two-way analyses of variance, with "nap
timing" and "response to TSD" as factors. The variations
in HAMD-6 scores were analyzed by means of Wilcoxon's
test. Correlational analyses were performed by computing
product-moment correlation coefficients. The level of significance was set at p < 0.05 (two-tailed).
Characteristics of Nap Sleep
aot~ 2 u~,.,,u~.s morning and afternoon nap sleep. Naps
at 9:00 AM and 3:00 PM did not differ in any of the sleep
parameters. Responders to TSD exhibited significantly less
M. Wiegand et al
Table I. Clinical Description of the Study Samplea
Male/female ratio
Mean HAMD-21 baseline
score ( ± SD)
Respoaders to TSD
Nonresponders to TSD
Naps at
9:00 AM
(n = 13)
Naps at
3:00 PM
(n = 15)
Naps at
9:00 AM
(n = 8)
Naps at
3:00 PM
(n = 11)
Naps ai
9:00 AM
(n = 5)
Naps at
3:00 PM
(n = 4)
2/I !
51.1 ± 10.6
28.5 ± 5.6
46.5 __ 12.9
25.7 +- 5.3
52.5 -- 12.3
28.5 -- 4.8
48.5 -+ 11.8
26.5 -- 5.6
48.8 _+ 7.9
28.6 +- 7.3
4 1 . 0 - + t5.9
23.8 -- 4.3
~TSD. total sleep deprivation; HAMD-21, Hamilton Depression Scale, 21-item version.
bANOVA, analysis of variation results (with factors "nap timing" and "response to TSD"); NS, not significant.
REM sleep and a lower REM density than nonresponders.
Results did not change when analyzing the relative instead
of the absolute amounts of sleep stages.
Influence of Nap Timing and Preceding Response
to TSD on Mood Changes
Figure 1 describes the distribution of nap effects in the
morning and afternoon nap groups, separately for responders and nonresponders to TSD. Five of the responders who took a nap at 9:00 AM exhibited severe
relapse into depression. In contrast, afternoon naps induced only slight (if any) worsening in re,ponders to TSD,
with the exception of one patient who showed a dramatic
deterioration in mood. A significant difference in the relapse rate between morning and afternoon naps occurred
in responders to TSD [Fisher's exact test comparing rate
of r~'lapse (nap effect ->4) with rate of nonrelapse (nap
effect <4; p = 0.041, two-tailed]. An analysis of variance
(Table 2, bottom) reflected the same trend for the nap
effect, yet did not yield significant differences with regard
to the factors "nap timing" and "response to T'SD."
R e l a t i o n x h i n A m n n o0 M o n r l C h a n o a ~
. . . . .
Duration, Content of Slow-Wave Sleep, and
Content oJ REM Sleep
Figure 2 demonstrates the relationship between nap sleep
duration (total sleep time) and the effect on mood. The
two parameters are negatively correlated; the coefficient
is significant for the total sample, indicating that longer
naps had less effect on mood. A separate analysis for
morning and afternoon naps (Table 3) showed that this
relationship was (nonsignificantly) more pronounced in
afternoon naps. Neither the amount of REM sleep during
a nap nor the content of slow-wave sleep was related significantly to its clinical impact.
A separate analysis was dedicated to the question of
whether the occurrence versus absence of REM sleep,
irrespective of its duration, might influence the clinical
impact of a daytime nap. Naps containing REM sleep
(n = 11 in the total sample) led to virtually no mood
changes (AHAMD-6, 0.6 __. 3.6 points), whereas naps
without REM sleep (n = 17) induced a mood worsening
(AHAMD-6, 3.2 ___ 4.1 points); however, the difference
did not reach levels of significance. The trend was more
pronounced in afternoon naps, which induced a mean mood
improvement when REM sleep was present (AHAMD-6,
0.5 _+ 2.6 points) in contrast to naps without REM sleep
(AHAMD-6, 3.1 _+ 4.7 points). Naps containing REM
sleep were significantly longer than naps without REM
sleep (85. l _+ 47.2 min versus 29.0 +_ 22.1 min, respectively; p < 0.001, Wilcoxon's test, two-tailed).
Relationship Between Nap Effect and the
Preceding Course of Mood
Figure 3 describes the course of depression ratings for
each responder to TSD during the days before and after
TSD, separately for the morning (upper part) and afternoon
(lower part) nap group. Again, the induction of clear mood
worsening by morning naps in the majority of TSD responders is evident (p < 0.01; Wilcoxon's test, two-tailed).
Afternoon naps, in contrast, led to slight changes in mood
(nonsignificant). In one case only was a release induced.
Although the patients had been randomly assigned to
the 9:00 AM versus 3:00 PM nap condition, the afternoon
nap group exhibited more pronounced morning/afternoon
variation in mood on the preceding day than the morning
nap group; however, the difference did not reach levels
of significance (see Table 2). There was no overall correlation between morning/afternoon variation in mood on
the preceding day and the nap effect (Table 3); however,
in the afternoon nap group, the correlation was nonsignificantly negative.
Baseline HAMD-2i scores, as well as age, turned out
to be uncorrelated with the nap effect. Patients with recurrent depression did not differ from those with a single
episode with regard to the frequency of relapses.
Naps After Sleep Deprivation in Depression
Table 2. Nap Sleep, Nap Effect, and MominodAfternoon Variation in Mood: Comparison of Morning Versus Afternoon Naps and
Responders Versus Nonresponders to Total Sleep Deprivation (TSD)
Naps at
9:00 AM
Nap sleep
Total sleep time
Sleep onset latency
Sleep efficiency (%)
Stage 0 (rain)
Stage 1 (min)
Stage 2 (rain)
Slow-wave sleep
REM sleep (min~
Naps w i t h R E M
sleep (n = 11)
REM sleep (min)
REM latency
REM density
Nap effect and variation
of mood
Nap effecff
variation of m o o d :
Responders to T S D
Naps at
3:00 PM
Naps at
9:00 art
Nonresponders to T S D
Naps at
3:00 .*M
Naps at
9:00 AM
Naps at
3:00 PM
n = 13
41.6 --. 38.1
n = 15
59.3 ± 47.5
n = 18
45.6 ± 46.1
n = !1
59.2 ± 42.2
n = 5
35.1 ± 23.3
59.5 ~ 67.8
9.7 ± ~ 6
9.1 ± 7.6
8.9 ± 4.9
9.0 ± 8.6
I I . 0 ± 6.9
9.1 - 4.1
± 29.7
~ 10.4
+ 9.4
_ 16.8
"4- 21.8
24.? _ 30.8
5.9 ± 9.9
n = 5
9.1 ± 17.9
n = 6
3.8 ± 6.8
n = 3
3.4 ± 5.4
n = 4
15.4 ± 10.6
25.3 ± 29.9
22.8 ± 22.8
37.0 ± 22.2
10.2 ± 7.9
15.7 ± 36.3
9.4 ± 4.9
49.6 ± 10.9
37.1 ± 28.7
n = 13
25.1 ± 17.4
n = 15
20.7 ± 10.1
n = 8
15.6 ± 9.4
n = 11
n = 5
1.7 ± 4.4
- 2 . 7 _ 3.8
1.2 ± 1.6
- ! . 2 ± 1.3
1.5 _ 4.7
- 1 . 3 ± 3.2
2.8 ± 3.8
- 1 . 1 ± 3.2
1.7 --- 4.3
- 2 . 3 ± 3.6
3.9 ± 4.5
- 1 . 0 ± 4.1
9.3 ± 13.9
n = 2
°ANOVA, analysis of variation results (with factors "nap timing" and "'response to TSD"); NS, net significant.
bMain effect for response to TSD (F = 18.7, df = 1, p = 0.003).
~Main effect for response to TSD (F = 18.6, df = 1, p = 0.003).
amain effect for response to TSD (F = 12.2, df = I, p = 0.01).
"Nap effect: difference of HAMD-6 ratings after vs. before the nap.
rMoming2afternoon variation of mood: difference of HAMD-6 ratings between 9:00 AM and 3:00 PM on the day before TSD.
A daytime nap can reinduce depressive symptomatology
in depressed patients who have improved by means of
TSD. Thus far, the present results confirm the clinical
impressions and ,~
_.4~.. ..o of some of .h.. vnr,=,~in,
. . . . . . .i~
. . .~.m. .d i ~
mentioned above, including data from our previous study
obtained in naps at 1:00 PM (Wiegand et al 1987b). In
responders to TSD, relapse and slight worsening were
more frequent than improvement. This clearly differs from
observations in healthy subjects, who in general benefit
by a nap toiiowing sleep deprivation (Taub et al 1976;
Naitoh 1981).
It might be objected that mood worsening may mirror
"sleep inertia" effects occ.rring immediately after awakening (Naitoh 1981); however, ratings were performed
approximately 30 min after wake-up; after such a delay,
sleep inertia effects are expected to be marginal (Webb
and Agnew 1974). In particular, the severe relapses that
we observed exceeded the range of slight, temporary discomfort that may be the expression of sleep inertia.
The timing of a nap appeared to be important to its
effect on depressive symptomatology. Morning naps had
the most detrimental impact in responders to TSD, whereas
afternoon naps were better tolerated. This finding differs
from the results of Gillin et al (1989) who found no difference in the (mostly beneficial) clinical effects of morning versus afternoon naps; howevcr, these naps were very
short (10 min). The study b:/ Kraft et al (1984) was restricted to seven patients who took afternoon naps; they
observed a relapse in only one case, which is in accordance
with our findings.
The difference between morning and afternoon naps
with regard to the impact on depression seems to support
those theories that emphasize the: role of circadian factors
and suggests that there may be a circadian variation in
propensity to relapse into depression. In analogy to the
"internal cohacidence model" (We,hr and Wirz-Justice 1981),
it may be sFeculated that a nap at 9:00 in the morning
interferes with a "vulnerabl(" or "critical phase," during
which the occurrence ,ff sleep is depressiogenic. The importance of circadian factors in the effects of sleep dep-
M. Wiegand et ai
5 - "
. . . . . . . . . . . . . . . . . . . . . . . . .•e................................................
• ......
Nonmsponders I
Figure I. Effects of morning and afternoon naps in responders
and nonresponders to TSD; Nap effect = AHAMD-6 prenap
versus postnap; 09:00, 9:00 AM; 15:00, 3:00 PM
rivation is further underscored by the observation that the
presence of a positive diurnal variation in mood is among
the few predictors of response to "ISD that have been
identified (Reinink et al 1990; Riemann et al 1991); however, the concept of a "critical phase" has recently been
questioned by the data of Southmayd et al (1990) who
demonstrated that relapses during the recovery night following successful TSD are not confined to a distinct period
of time.
Moreover, in the present analyses, timing of naps is
not independent of the duration of prior wakefulness because the sleep deprivation periods began consistently at
7:00 AM on the preceding day. Thus, the more detrimental
impact of morning naps could alternatively be explained
by the S-deficiency hypothesis: Following this model, after
continuous sleep deprivation, the deficient "process S" will
have a higher level in the afternoon than in the morning,
and an afternoon nap will be less likely to reduce process
S to a degree leading to recurrence of depressive symptoms, compared with a morning nap where even small
amounts of sleep may be sufficient to reinduce depression.
Thus, our finding that nap timing is crucial to its effect
on mood does not necessarily favor circadian models but
is compatible with "homeostatic" explanations (e.g., as
provided by the process S theory).
In a similar way, Wu and Bunney's (1990) model can
serve to explain the difference between morning and afternoon naps: If a hypothetical "depressiogenic substance" is
metabolized during wakefulness in a linear, time-dependent way, longer preceding wakefulness would lead to
lower levels of this substance, and relapse would be less
likely in the afternoon because the baseline level of the
substance should be lower. Future studies in this field
should especially attempt to separate the influences of nap
timing and duration of prior wakefulness to allow the separation of "circadian" and "homeostatic" influences.
We cannot exclude the possibility that the less harmful
impact of afternoon naps is due to an accidental difference
in the course of depression on the preceding day: The
afternoon nap group tended to exhibit a more pronounced
morning/afternoon variation in mood that correlated negatively (not reaching levels of statistical significance) with
the nap effect; in addition, these patients tended to have
lower HAMD-6 scores before the nap. On the other hand,
Figure 3 demonstrates that even those patients who had
exhibited a less pronounced positive diurnal variation with
high depression levels in the preceding afternoon either
improved or showed minor worsening following an at,ernoon nap on the next day.
Both the S deficiency and the depressiogenic substance
model would predict that independent of nap timing, relapses into depression are more likely to occur following
longer naps. In the pilot study by our group of naps at
1:00 PM (Wiegand et al 1987b), there was indeed a tendency for longer naps to have a less favorable impact on
depressive symptomatology. The present data do not support this finding and even point to the opposite direction:
Longer naps were better tolerated, and this result was more
p~,~ounced following afternoon naps; however, after very
brief naps ( < 10 min duration), we did not observe relapse,
which is in agreement with the findings of Gillin et al
(1989) but disagrees with the observation by Roy-Byrne
et al (1984) of an ultrashort (90 sec) nap followed by a
severe relapse, as well as with the report by Southmayd
et al (1987). It can be summarized that very long naps do
not seem to be more detrimental than shorter ones. The
existing evidence contradicts the assumption of a linear
relationship in either direction between nap length and
clinical effects and thus is not compatible with the respective predictions of the S-deficiency and depressiogenic
substance models.
In accordance with Gillin et al (1989), we did not find
differences in sleep variables between morning and afternoon naps. In particular, there was no indication of increased REM sleep pressure in morning versus afternoon
naps, as could be expected from data by Kupfer et al
Naps After Sleep Deprivation in Depression
-.apt at 09:oo (.='t 3}1
* naps at
12= -.42,
p < O.05X
•4 , . . . . . . . . . . .
"0 .........................
'0" . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
[Total s l e e p _ t i m e ( m i n ~
Figure 2. Nap effect and nap sleep duration; Nap effect = AHAMD-6 prenap versus postnap; 09:00,
9:00 AM; 15:00, 3:00 PM.
Table 3. Correlation of Nap Effect with Age, Psychopathology, and Sleep Variables"
C o ~ e ! a t i o n of , u p
effect with
(n = 28)
(n = 19)
Age (yr)
- 0.08
Baseline H A M D - 2 !
- 0.20
- 0.12
M o m i n g , ' a f t e m o o n variation
Naps at
9:00 AM
(n =
Naps at
3:00 PM
R e s l ~ r , ders
(n = 8)
(n = 15)
(n = I1)
- 0.12
- 0.51
- 0.49
- 0.47
- 0.24
in mood
Total sleep time ( m i n )
- 0.42 b
- 0.30
- 0.27
- 0.32
- 0.47
S l o w - w a v e sleep ( m i n )
- 0.20
- 0.06
- 0.29
- 0.40
- 0.14
R E M sleep (min)
o~od,ct.-moment co__rre_!ationcoefficients: HAMD-21. Hamilton Depression Scale, 21-item version; REM, rapid eye movement.
"p < 0.05, two-hailed; all other coefficients not significant.
( 1981 ). It is remarkable that in naps containing REM sleep,
despite the preceding TSD, mean REM :atencies at both
nap time points are rather short. This is not in agreement
with the expectation derived from the two-process model
of sleep regulation that after sleep deprivation, the rebound
of slow-wave sleep should prevent an early onset of REM
Responders to TSD differed from nonresponders with
regard to REM sleep variables: They exhibited less REM
sleep and lower REM density (a prolonged REM latency
failed to reach statistical significance). Sleep structure of
daytime naps thus seems to reflect the clinical condition,
with nonresponders to TSD exhibiting a more "depressive"
sleep paUern; however, with respect to the relatively small
number of naps containing REM sleep (n = 11), these
findings should be regarded as preliminary. In nocturnal
sleep following TSD, Riemann and Berger (1990) failed
to find significant differences in REM sleep variables between responders and nonresponders.
Similar to our pilot study of naps at 1:00 PM, the total amount of slow-wave sleep during a daytime nap
showed no ~lationship with clinical effect. This does not
support the respective expectation derived from the Sdeficiency theory. For any critical test of this hypothesis, however, EEG power spectra wotild be required
(which were not available in the present study) because
M. Wiegand et al
'* T/
momln~l 1.qq
nap /
ITotol sl~p d~xivai~ I
Figure 3. Course of depression ratings in responders to TSD; upper part, morning nap group; lower
part, afternoon nap group; 15:00, 3:00 PM, 17:00, 5:00 PM.
the amount of visually scored slow-wave sleep can be
expected to correlate with EEG delta power (Brunet et
al 1988). Consequently, some type of relationship should
be present between the amount of slow-wave sleep and
mood worsening; however, this is not evidenced by our
The chollnergic-amincrgic imbalance model should
predict the occurrence and amount of REM sleep to be
related with clinical effect; this expectation, too, was not
confirmed by our data. Moreover, our findings agree with
a recent study by Riemann et al__(in,___~-nress', preliminary
results published in Riemann et al 1989), which aimed
directly at comparing morning naps containing REM sleep
with morning naps without REM sleep and found no differential effects on mood. In contrast, in our former pilot
study of naps at 1:00 PM, naps containing REM sleep
tended to be more detrimental. Thus, the h~T,othesis derived from the cholinergic-aminergic imbalance model of
depression that cholinergic overactivity may be involved
in relapses into depression caused by a daytime nap is not
supported by the data with respect to naps at 9:00 AM and
3:00 PM. An open question remains as to how far, due to
circadian variations in cholinergic functioning, REM sleeprelated mo,:,d worsening is restricted to naps taken at approximately l:00 I'M.
It must be concluded that the relationship between nap
sleep and its impact on depressive symptomatology does
not appe~,r to be linear and univariate. This is i., agreement
with llie conclusions by Southmayd et al t1990). Even
when considering the clear differences in relapse rates
between morning and afternoon naps, the large variety of
clinical effects within each experimental subgroup requires
explanation. A multifactorial model would probably fit
better with the existing evidence. As a trait factor, there
may be a differential sensitivity in each individual patient
to manipulations of the sleep--wake cycle that may be
manifested in the frequency and intensity of diurnal variatlnn~ in mood, in tho nrnh2hil;tw of response :-LSJ TSD, ~-~
~4g,ltlh¢ I ~ r , K ~ , , C L I I b 6 1 , , J , I I , & & L I I ~
in a differential "vulnerability" to the impact of sleep on
depressive symptomatology following successful sleep
deprivation. St~cond, some circadian or ultradian factor
may manifest itself in one or more "critical phases," during
which sleep is more likely to promote depression. This
factor may interact closely with "homeostatic" influences,
as suggested by the process S model, the depressiogenic
substance theory and the cholinergic-aminergic imbalance
hypothesis; however, considerably larger samples would
be required to study the complex interactions within such
a multifactorial model.
To summarize, our main findings are essentially compatible with all major hypotheses that undertake to explain
the unfavorable impact of sleep on depression, and they
do not clearly refute any of them; however, none of these
hypotheses appears to sufticie~tly cover every aspect of
Naps After Sleep Deprivation in Depression
the observations. Relapses caused by daytime naps seem
to result from complex interactions of several factors; simple and linear relationships between single variables and
clinical effects appear to be improbable.
We gratefullyacknowledgethe help of Mrs. Ursula Hofer(~search n ~
at the Max Planck Institute of Psychiatry), Mrs. Gaby Reim (research
nurse at the Central Institute of Mental Health), as well as the assistance
of Matthias Junker and Stephan Sto|z.
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