J Autism Dev Disord (2008) 38:1625–1633
DOI 10.1007/s10803-008-0543-0
ORIGINAL PAPER
Sleep Patterns in School-age Children with Asperger Syndrome
or High-functioning Autism: A Follow-up Study
Hiie Allik Æ Jan-Olov Larsson Æ Hans Smedje
Published online: 22 February 2008
Ó Springer Science+Business Media, LLC 2008
Abstract The course of sleep patterns over 2–3 years was
compared between 16 school-age children with Asperger
syndrome (AS) or high-functioning autism (HFA) and 16 age-
and gender-matched typically developing children, using
1-week actigraphy at baseline and follow-up. At baseline
(mean age 11.1 years), children with AS/HFA had longer
sleep latency and lower sleep efficiency during school days,
but earlier sleep start and sleep end during weekends. At
follow-up (mean age 13.7 years), children with AS/HFA had
longer night wakings and lower sleep efficiency during
weekends than the controls. The overall change of sleep pat-
terns, however, is similar in children with AS/HFA and
typically developing controls over a 2 to 3-year period.
Keywords Asperger syndrome
High-functioning
autism
Longitudinal sleep
Actigraphy
Introduction
Disturbed sleep is considered common in school-age chil-
dren with Asperger syndrome (AS) and high-functioning
There is one change in affiliation since the time of the study, namely,
Hiie Allik has defended her thesis, and obtained a doctoral degree at
the Karolinska Institutet, Stockholm, Sweden. Dr. Allik conducted
this study in partial fulfilment of the requirements for a doctoral
degree at the Karolinska Institutet, Stockholm, Sweden.
H. Allik (&)
J.-O. Larsson
Department of Woman and Child Health, Karolinska Institutet,
Child and Adolescent Psychiatric Unit, Q3:O4, Astrid Lindgren
Children’s Hospital, 171 76 Stockholm, Sweden
e-mail: hiie.allik@ki.se
H. Smedje
Department of Neuroscience, Uppsala University, Child and
Adolescent Psychiatric Unit, 751 85 Uppsala, Sweden
autism (HFA) (Couturier et al. 2005; Paavonen et al.
2007). However, several issues pertaining to the topic of
sleep in individuals with these diagnoses remain under-
researched. Longitudinal studies which compare the course
of sleep pattern in children with AS/HFA and in children
with typical development are lacking in the existing liter-
ature (Honomichl et al. 2002).
Approximately 0.3% of children who attend mainstream
schools fulfil criteria for pervasive developmental disorders
(PDD), among them AS and HFA (Scott et al. 2002; Webb
et al. 2003). AS and HFA is considered to be often associ-
ated with coexisting behavioral or psychiatric disorders
(Ghaziuddin et al. 1998), including sleep disturbance (Allik
et al. 2006b, c; Couturier et al. 2005; Oyane and Bjorvatn
2005; Paavonen et al. 2003; Patzold et al. 1998; Richdale
and Prior 1995; Tani et al. 2003; Wiggs and Stores 2004). It
has even been suggested that sleep disturbance may consti-
tute a salient feature of the AS/HFA phenotype (Limoges
et al. 2005; Richdale and Prior 1995).
Cross-sectional studies indicate that difficulties initiating
and maintaining sleep are particularly common types of sleep
disturbances in children as well as in adolescents and adults
with AS/HFA (Couturier et al. 2005; Paavonen et al. 2007;
Patzold et al. 1998; Richdale and Prior 1995; Tani et al. 2003;
Wiggs and Stores 2004). Previous studies based both on
subjective (Paavonen et al. 2007; Patzold et al. 1998; Rich-
dale and Prior 1995) and objective sleep measures (Allik et al.
2006b, c; Godbout et al. 2000; Wiggs and Stores 2004) of
children with high-functioning PDD have indicated that there
are aberrations in sleep patterns. The findings of these studies
have included longer sleep latencies, more frequent and
longer night-time awakenings, shorter sleep duration and
earlier morning awakenings compared to controls.
Sleep research on adults with AS/HFA has also been per-
formed. Tani and colleagues reported that insomnia was
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common in individuals with AS according to subjective report
(Tani et al. 2003), but not according to actigraphy (Tani et al.
2005) or polysomnography (PSG) (Tani et al. 2004). In
another study, Limoges et al. (2005) found a high frequency
of sleep disturbance in adolescents and adults with AS/HFA
according to both sleep questionnaire and PSG, despite no
report of subjective sleep complaints. Similarly, Oyane and
Bjorvatn (2005) reported tendencies towards actigraphy-
recorded sleep disturbance in young adults with AS/PDD.
Thus, existing cross-sectional studies indicate that sleep
disturbance related to sleep timing, duration, initiation, and/or
maintenance is very common at all ages in AS/HFA. How-
ever, only a few studies have followed these individuals
longitudinally. One study which assessed the short-term sta-
bility of sleep patterns in PDD, conducted by Honomichl et al.
(2002) was based on a diary and sleep questionnaire and
included eight children with AS/HFA in the sample. The
authors found a high persistence of sleep-wake problems
across a 3-month-period, and pointed out the great need for
further longitudinal research of sleep in childhood PDD.
Longitudinal investigations of the sleep development in
typically developing children have, among other alterations
highlighted the following changes over the course of time: a
delay of the timing of the sleep phase; a reduction of the total
sleep duration, and an increasing difference between the
school day and the weekend sleep schedules (Carskadon
1990; Laberge et al. 2001). Notably, however, these longitu-
dinal studies were based on subjective measures. There are a
few long-term studies which are based on PSG (Anders and
Keener 1985), and there is a scarcity of longitudinal acti-
graphic studies. To the best of our knowledge only one
previous report has published longitudinal actigraphic data on
young children from early childhood (Scher et al. 2004), and
longitudinal actigraphic data on school-age children seems to
be lacking. However, short-term actigraphic studies con-
ducted on school-age children have been performed, and they
have confirmed age- and gender-related differences in sleep
patterns (Gaina et al. 2004, 2005; Sadeh et al. 2000).
Fig. 1 Sleep assessment AS/HFA group
procedure at T1 and T2 in
children with AS/HFA and Base line 16 children (14 boys, 2 girls)
controls. Interval between
T1 and T2 was: 2.5 (range Time 1 (T1)
2.2–3.7 years) for all these 32
children (16 with AS/HFA and
16 controls). The mean
difference in follow-up time
between children within
each pair was 18.5 days
(range 7.0–37 days)
Follow-up 16 children (14 boys, 2 girls)
Time 2 (T2)
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J Autism Dev Disord (2008) 38:1625–1633
We have previously used diary and actigraphy to compare
the sleep patterns between 32 school-age children with AS/HFA
and 32 age- and gender-matched controls (Allik et al. 2006c). In
the named study both subjective and objective sleep measures
showed moderate differences between the two groups; the
children with AS/HFA had earlier bed- and get up times on
weekends, longer sleep latencies both on school days and
weekends, and lower sleep efficiencies on school days. In the
present study, performed on a subsample of these children
consisting of 16 matched pairs of children with AS/HFA and
controls, we focus on the course of actigrahic sleep patterns
from baseline to follow-up, 2–3 years later. The main objectives
of the study were to determine: (a) if differences in sleep pat-
terns, more specifically, the timing, initiation, and maintenance
of sleep, observed at baseline are evident also at follow-up, and
(b) whether the course of sleep patterns from baseline to follow-
up, differs between the children with AS/HFA and the controls.
Methods
Participants
Sleep patterns of school-age children with AS/HFA were
compared to those of age- and gender-matched typically
developing children at baseline (Time 1, T1) and at follow-up
(Time 2, T2). The study sample consisted of 16 matched pairs,
14 boys and 2 girls derived from an initial sample of 32 matched
pairs. The initial sampling procedure has been described in
previous papers (Allik et al. 2006a, b, c). Twenty-one out of the
32 children with AS/HFA, and 20/32 controls from the initial
sample were available for follow-up at T2. However, 5 of the 21
children with AS/HFA and 4 of the 20 controls participated
without their corresponding pairs at T2, and in order to retain a
pairwise matched design, these 9 children were not included in
the present report. Thus, the present study sample consisted of
16 matched pairs, which were measured twice, at T1 and T2
(Fig. 1).
Control group
16 matched pairs 16 children (14 boys, 2 girls)
Measures: One-week actigraphy (16 vs 16)
16 matched pairs 16 children (14 boys, 2 girls)
J Autism Dev Disord (2008) 38:1625–1633
There were no statistically significant differences
between the participants who remained in the study at T2
and the drop-outs who only participated at T1 in regards to
the seven measures of sleep analysed in this paper with the
exception for sleep efficiency. Those who remained in the
study had somewhat higher sleep efficiency on school days
at T1 than the drop-outs; 85.6% versus 88.7%; p \ 0.01
(t-test for independent samples).
The mean age of children with AS/HFA was: 11.1 years
(range 8.5–12.9) at T1 and 13.7 years (range 11.7–15.5) at
T2, and of the controls: 11.2 years (range 8.5–13.4) at T1
and 13.7 years (range 11.2–15.6) at T2. The mean interval
between T1 and T2 for 32 children (16 children with
AS/HFA and 16 controls) was 2.5 years (range 2.3–3.7).
Within matched pairs, the mean difference in follow-up
time between the child with AS/HFA and the control child
was 18.5 days (range 7.0–37 days).
During the initial sampling procedure, the families were
informed that the study aimed to explore sleep patterns, and,
importantly, presence of comorbid physical disabilities or
pharmacological treatment, factors known to potentially
affect sleep (Mindell and Owens 2003a, b), constituted
exclusion criteria at T1. However, at T2 we included all
children/families that were willing to remain in the study.
Consequently, three children in the AS/HFA group, versus
two children in the control group with medical problems were
included at T2 [AS/HFA: allergic symptoms (n = 2); allergy
and insulin-dependent diabetes (n = 1) starting around
1.5 years before the T2; versus control group: allergic
symptoms (n = 2)]. Moreover, three children with AS/HFA
and two of the controls received pharmacological treatment at
T2 [AS/HFA: anti-asthma medication (n = 1), anti-asthma
medication and melatonin (n = 1), insulin and anti-asthma
medication (n = 1) versus control group: anti-asthma medi-
cation (n = 2)].
Measures
Actigraphy
Actigraphs (Actiwatch, Cambridge Neurotechnology, Ltd.,
Cambridge, UK), worn on the child’s nondominant arm
during 1 week, recorded all movements exceeding the 0.05 g
threshold and translated these movements into electrical
signals. Data were collected at the medium sensitivity level
with the epoch length 30 s and stored as activity counts per
epoch in the Actiwatch’s 16-K memory. Data from the act-
igraph’s memory were thereafter downloaded to the
Actiwatch Sleepwatch software (The Actiwatch Activity
Monitoring System 1999). Bed- and get up times, recorded by
children and parents parallel to actigraphic assessment, were
manually entered into the software program, and the
1627
following actigraphic sleep measures were calculated: sleep
start (the first minute after bedtime that was identified as
sleep by the Actiwatch Sleepwatch algorithm, and followed
by at least 10 consecutive minutes of recorded immobility),
sleep latency (the latency before sleep start following bed-
time), sleep end (the last epoch of immobility before the start
of at least 10 min of consecutive activity), actual sleep time
(the difference between sleep end and sleep start in minutes
minus actual time spent awake during the sleep period), and
sleep efficiency (the percentage of time spent asleep while in
bed). In addition to the data automatically generated from the
Actiwatch Sleepwatch software, number of night wakings
(wakings lasting 5 min or longer, preceded and followed by
at least 15 min of uninterrupted sleep, which are scored
manually from the actigraph data (Allik et al. 2006c)), and
duration of night wakings (the total duration of these wa-
kings C 5 min) were calculated. The child/parent-recorded
bed- and get up times showed good correlations to sleep start-
and sleep end times, Pearson product moment correlation
coefficients ranging between 0.92 and 0.99. Therefore, only
actigraphic data are presented in this report.
Procedure
Both at T1 and T2, the first author visited families in their
homes and distributed the actigraphs. Participants and their
parents were instructed on the use of actigraphs and how to
write down the child’s daily bedtime and get up time.
Actigraphic recording commenced in conjunction with this
home visit and was conducted for 1 week. Following the
monitoring period, actigraphs were returned to the first
author via a second home visit. At T1, the paired off
children were examined within 2–4 weeks of their coun-
terpart using the same actigraphy device (n = 4) (Allik
et al. 2006c). Fifteen children with AS/HFA and 16 chil-
dren from the control group were monitored for 7 days, and
one child with AS/HFA was monitored for 6 days at T1.
The pairings were also maintained at T2. Hence, 16 pairs of
children were examined within 2–4 weeks using the same
actigraphy device (Fig. 1). At follow-up, 14 children with
AS/HFA versus 10 of the controls were monitored for
7 days, one child with AS/HFA versus five of the controls
were monitored for 6 days, and one child with AS/HFA
versus one of the controls were monitored for 5 days.
Statistical Analysis
All analyses of actigraphic data for each child were averaged
into school day and weekend mean values, using the occur-
rence of school attendance the next day as the definition
of a school day (school day: Sunday, Monday, Tuesday,
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Wednesday, Thursday; weekend: Friday, Saturday). Further,
in order to examine the development of sleep pattern, a sep-
arate new variable, change (T2 T1 difference) was calculated.
T-tests for paired samples were used to conduct group com-
parisons of the mean values at T1 and at T2, as well as change.
In order to measure the levels of change within the AS/HFA
group and within the control group, one-sample t-test was
conducted. A significance level of p \ 0.05 was regarded as
statistically significant (SPSS base 9.0 User’s guide 1999).
The study was approved by The Ethical Committee at
the Karolinska Hospital, Stockholm, Sweden.
Results
Table 1 provides the actigraphy data for T1 and T2, and the
T1 T2 difference, change.
Figure 2 provides graphic illustration of the course of
sleep patterns.
Timing of sleep was assessed by ‘‘sleep start’’ and ‘‘sleep
end times,’’ duration of sleep by ‘‘actual sleep time,’’ initiation
of sleep by ‘‘sleep latency,’’ and maintenance of sleep by the
‘‘number of night wakings (C5 min),’’ ‘‘duration of night
wakings (C5 min),’’ and ‘‘sleep efficiency.’’
Baseline (T1)
Baseline sleep data for 32 children with AS/HFA and 32
typically developing controls are presented in our previous
report (Allik et al. 2006c). The present report includes
merely 16 of these 32 matched pairs. At T1 (mean age
11.1–11.2 years), the two groups differed with respect to
timing, initiation, and maintenance of sleep. The AS/HFA
group showed 42 min earlier sleep start times (weekend),
60 min earlier sleep end times (weekend), longer sleep
latencies (school day), and lower sleep efficiencies (school
day) than the control group. Sleep duration did not differ
between the two groups at T1.
Follow-up (T2)
At T2 (mean age 13.7 years), the AS/HFA group had
longer lasting night wakings and lower sleep efficiencies
during weekends than the controls. Timing, initiation, and
duration of sleep did not differ between the groups.
Change, T2–T1 Difference
As shown in Table 1 and Fig. 2, there was no difference
between the two groups across the 2 to 3-year period
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regarding the change of the sleep timing, initiation, dura-
tion, and maintenance variables. With respect to the timing
of sleep, both the children with AS/HFA and the controls
displayed a sleep phase delay, approximately 40 min
delayed sleep start times for the whole week, and 16–
39 min delayed sleep end times during weekends. Sleep
duration during school days decreased by approximately
80 min in both groups and the corresponding decrease
during weekends was 43–56 min. Moreover, in both
groups, sleep efficiency decreased by 7–10%.
Discussion
The present study assesses whether over the course of 2–3
years sleep patterns develop differently in school-age
children with AS/HFA as compared to typically developing
children in a matched control group. The investigation,
which is based on actigraphic sleep measures, extends our
previous work by exploring sleep in childhood AS/HFA
longitudinally. Main findings indicate that individuals with
AS/HFA displayed subtle aberrations in sleep timing,
initiation, and maintenance at baseline, and aberrations in
sleep maintenance at a 2 to 3-year follow-up. These short-
term aberrations in sleep timing, initiation and maintenance
remain to be tested and further explicated in future larger
studies. Importantly, however, essential aspects of the
longitudinal course of sleep pattern were similar in the
children with AS/HFA and in the typically developing
controls. Both the children with AS/HFA and the controls
demonstrated similar age-related trajectories in their sleep
development, mainly a sleep phase delay and a shortening
of sleep duration.
To the best of our knowledge, there are no previous
longitudinal sleep data for school-age children with AS/
HFA. Thus, we need to attempt compare our current long-
term sleep data with findings from previous cross-sectional
studies.
Short-term aberrations in sleep timing in AS/HFA were
found in the current study; the children in the AS/HFA
group fell asleep 42 min earlier and woke up 60 min earlier
than the children in the control group during weekends at
baseline, but not at the 2 to 3-year follow-up. The present
data also indicate that the development of sleep timing over
a 2 to 3-year period in children with AS/HFA compared to
typically developing children is more or less the same.
Previous cross-sectional research on children (Richdale
and Prior 1995) and adolescents/adults with AS/HFA
(Limoges et al. 2005) has also provided some evidence for
aberrations in sleep timing. For example, studies by
Richdale and Prior (1995) and by Limoges et al. (2005)
have reported earlier bed- and/or get up times in children
and adolescents/adults with AS/HFA or high-functioning
 Table 1 Actigraphy measures of 16 children with Asperger syndrome (AS)/high-functioning autism (HFA) and 16 children in the control group at baseline and follow-up
Sleep variable Day Baseline (T1) Follow-up (T2) Change (T2 T1 difference)
1 2
Mean, SD AS/HFA Control p AS/HFA Control p AS/HFA p3 Control p4 p5
J Autism Dev Disord (2008) 38:1625–1633

Sleep start School day 09:47 (40.5) 09:51 (25.7) 0.51 10:31 (55.6) 10:35 (23.7) 0.67 45.0 (39.6) \0.001 45.9 (22.4) \0.001 0.94
Time (PM) (SD-min) Weekend 10:43 (54.8) 11:25 (54.7) 0.03 11:22 (68.1) 00:03 (55.8) 0.07 40.2 (57.3) 0.01 39.7 (47.8) \0.01 0.98
Sleep end School day 06:54 (28.7) 07:09 (15.9) 0.08 06:52 (27.8) 07:08 (36.7) 0.25 2.7 (21.8) 0.63 3.6 (34.2) 0.68 0.92
Time (AM) (SD-min) Weekend 07:44 (50.9) 08:44 (52.8) \0.01 08:22 (92.1) 08:57 (48.3) 0.15 38.8 (69.2) 0.04 15.9 (54.8) 0.26 0.29
Sleep latency School day 26.5 (13.2) 14.7 (10.7) 0.001 25.3 (22.1) 17.8 (11.3) 0.26 -0.4 (23.1) 0.95 3.2 (16.1) 0.43 0.62
Mean (SD-min) Weekend 18.4 (12.5) 13.2 (11.4) 0.59 28.1 (25.1) 14.2 (16.3) 0.13 8.4 (23.1) 0.16 1.2 (18.1) 0.78 0.28
Actual sleep time School day 511 (27.9) 522 (32.3) 0.27 434 (32.5) 445 (39.5) 0.49 -79.5 (35.4) \0.001 -81.0 (43.8) \0.001 0.89
Mean (SD-min) Weekend 506 (33.9) 523 (48.3) 0.18 462 (50.8) 465 (44.3) 0.64 -43.3 (41.3) 0.001 -56.0 (68.8) \0.01 0.31
Number of night School day 1.0 (0.8) 1.0 (1.0) 0.94 1.5 (0.8) 1.5 (0.7) 0.90 0.5 (0.8) 0.03 0.5 (1.2) 0.11 0.93
Wakings (C5 min) Weekend 1.1 (0.8) 0.8 (0.9) 0.42 2.3 (0.9) 1.6 (0.8) 0.05 1.2 (1.1) \0.001 0.8 (1.2) 0.02 0.29
Mean (SD)
Duration of night School day 9.3 (7.7) 7.2 (7.1) 0.18 14.4 (9.3) 15.1 (10.2) 0.86 5.1 (9.7) 0.05 7.8 (13.0) 0.03 0.48
Wakings (C5 min) Weekend 7.8 (5.9) 5.8 (6.0) 0.27 22.2 (10.6) 13.2 (7.1) \0.01 14.3 (11.8) \0.001 7.4 (9.1) \0.01 0.06
Mean (SD-min)
Sleep efficiency School day 88.7 (3.2) 91.2 (4.0) \0.01 81.8 (5.0) 83.5 (4.0) 0.17 -6.9 (5.2) \0.001 -7.3 (6.3) \0.001 0.76
Mean (SD-%) Weekend 89.9 (3.8) 91.1 (4.2) 0.16 79.5 (5.6) 83.4 (5.2) 0.05 -10.3 (5.7) \0.001 -7.9 (7.7) \0.01 0.15
p1, t-test for paired samples, AS/HFA versus controls at T1; p2, t-test for paired samples, AS/HFA versus controls at T2; p3, One-sample t-test, change in AS/HFA group from T1 to T2; p4, One-
sample t-test, change in controls from T1 to T2; p5, t-test for paired samples, change in AS/HFA group versus controls
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Fig. 2 The development of Sleep Latency Sleep Start

25
40
sleep patterns in 16 children
AS/HFA sd Controls sd AS/HFA sd Controls sd
with AS/HFA and 16 controls AS/HFA we Controls we AS/HFA we Controls we

Sleeplatency (minutes)

24
over a 2–3 year period.

30

Sleep Start
Abbreviations: sd, school day;
we, weekend

23
20

22
10

21
0
t1 t2 t1 t2
Time Time

Sleep End Actual Sleep

550
10
AS/HFA sd Controls sd AS/HFA sd Controls sd

Actual Sleep Time (minutes)

AS/HFA we Controls we AS/HFA we Controls we
9

500
Sleep End
8

450
7

400
6

t1 t2 t1 t2
Time Time

Number of Night Wakings Duration of Night Wakings

30
3

Duration Night Wakings (minutes)

AS/HFA sd Controls sd AS/HFA sd Controls sd
Number of Night Wakings

AS/HFA we Controls we AS/HFA we Controls we

2.5

20
2
1.5

10
1
.5

t1 t2 t1 t2
Time Time

Sleep Efficiency
95

AS/HFA sd Controls sd
AS/HFA we Controls we
Sleep Efficiency (%)
90
85
80
75

t1 t2
Time

PDD, compared to controls. Limoges et al. (2005) even
proposed that a subtle sleep phase advance, perhaps
reflecting atypical sleep architecture, may be a common
trait in individuals with AS/HFA. Present baseline findings
of a tendency towards earlier sleep phase at T1 are thus
partly consistent with data from previous cross-sectional
research. However, the issue of a sleep phase advance in
individuals with AS/HFA obviously needs further explo-
ration in longitudinal studies with larger samples.
It is also important to recognize that a tendency towards
earlier sleep phase among children with AS/HFA might
have other explanations than such that are related to sleep
architecture or sleep biology. One alternative explanation
could be that the earlier bedtime in AS/HFA reflects
environmentally dependant factors as parental practices
(Allik et al. 2006c). For instance, if parents of children
with AS/HFA tend to put them to bed earlier than parents
of children without AS/HFA, then the prolonged sleep
latency found in the children with AS/HFA could be due to
not being sleepy or tired enough to fall asleep at the earlier
bedtime. Notably, parenting a child with AS/HFA is often
time consuming and stressful, and an earlier bed time could
allow parents to catch up on all of those things they could
not do while looking after their child.
Sleep duration did not differ between the groups, neither
at baseline nor at follow-up, and both groups demonstrated

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similar shortening of sleep duration over time. These
findings are not in agreement with data from previous
cross-sectional studies on children with high-functioning
PDD (Paavonen et al. 2007; Patzold et al. 1998; Richdale
and Prior 1995) which have showed shorter sleep duration
in PDD compared to controls. However, the present results
do resemble findings on adults with AS/HFA in which
sleep duration was not found to differ from that of controls
(Limoges et al. 2005; Tani et al. 2003, 2005). The dis-
crepancy between our results and the results of previous
sleep research on children with PDD may stem from dif-
fering methodological design such as in the current study
different sample selection, the longitudinal approach, sep-
arate analyses of sleep before school day mornings and
before weekend mornings, and a control group of typically
developing children.
In the present study, longer sleep latency in AS/HFA
during school days was detected at T1, but not at T2, and
the change in sleep latency from T1 to T2 was similar
between two groups. Prolonged sleep latency has been
found consistently in previous cross-sectional studies, both
on children with AS/HFA (Paavonen et al. 2003, 2007;
Patzold et al. 1998; Richdale and Prior 1995) and on adults
with AS and/or HFA (Limoges et al. 2005; Tani et al.
2003). Furthermore, prolonged sleep latency has been
found to be more pronounced during working days than
during weekends in adults with AS (Tani et al. 2003). This
corresponds to the current finding of prolonged sleep
latency during the school days at T1 (Table 1).
Plausible explanations of prolonged sleep latency in
individuals with AS/HFA could be: anxiety, high physio-
logical arousal, more problematic daytime behaviour, and
fear (Limoges et al. 2005; Paavonen et al. 2003, 1998;
Richdale and Prior 1995; Tani et al. 2003). In our previous
report daytime behaviour was compared between children
with AS/HFA who had insomnia and those who did not
have insomnia (Allik et al. 2006b). Children with insomnia
had higher scores of autistic and emotional symptoms and
lower scores of prosocial behaviour in parent reports, and
teachers reported higher scores of hyperactivity and emo-
tional symptoms. As stated above, another explanation of
the prolonged sleep latency in the children with AS/HFA
might be that these children had earlier bedtimes than
children in the control group (Allik et al. 2006c).
Furthermore, impaired sleep maintenance in children
with AS/HFA was also found in the current study, i.e.,
lower sleep efficiency on school days at baseline, as well as
longer-lasting night wakings and lower sleep efficiency on
weekends at follow up (T2). These findings corroborate
findings of aberrant sleep maintenance in earlier cross-
sectional studies (Godbout et al. 2000; Limoges et al.
2005; Patzold et al. 1998; Richdale and Prior 1995). A
higher number and longer duration of nocturnal wakings
1631
was found in children with AS and/or HFA (Patzold et al.
1998; Richdale and Prior 1995) as well as in adults with AS
and/or HFA (Limoges et al. 2005), reflecting poorer sleep
maintenance. The studies by Richdale and Prior (1995) and
Patzold et al. (1998) demonstrated longer night wakings in
children with high-functioning PDD than in controls,
according to diary recordings. Limoges et al. (2005)
reported increased nocturnal awakenings (number and/or
duration) in adults with AS/HFA than in controls according
to self-report questionnaires and PSG.
In the current longitudinal study significant age-related
changes in the timing and duration of sleep was docu-
mented in children with AS/HFA as well as in typically
developing children in the control group. These findings
are well in line with existing research on typically devel-
oping children (Gaina et al. 2004; Laberge et al. 2001).
The current finding of a sleep phase delay, an average 40–
45 min in sleep start times for the whole week resembles
data from previous research (Laberge et al. 2001). Like-
wise, decreased sleep duration on school days and lower
sleep efficiency for the whole week at T2 that was found in
the current study (see Table 1 and Fig. 2) coincide with
data from previous actigraphy-based research on typically
developing children (Gaina et al. 2004).
To the best of our knowledge, this study might be the
first to provide longitudinal actigraphic sleep data on a
sample of school-age children. Actigraphy has been rec-
ommended for documentation of longitudinal changes in
sleep patterns or schedules (Lockley et al. 1999). Other
strengths of the current report pertain to our inclusion of
children with high-functioning PDD, limited age range,
and comparisons with a control group of typically devel-
oping children.
However, the current study has several limitations which
should be taken into consideration while interpreting the
results. It cannot be sure that the current results may be
generalized to children with AS/HFA in other settings
since the data were based on a relatively small sample of
children, only 16 matched pairs of children at baseline and
at follow-up. Two types of selection biases at T1 may have
affected the results. On the one hand, it is possible that
more families that have children with PDD and disturbed
sleep accepted the offer to participate in the study. On the
other hand exclusion criteria resulted in the selection of
healthier and non-medicated children at T1. Severely
sleep-disturbed children who received medication for sleep
problems may therefore have been excluded from our
initial sample. Hence, selection biases may have worked in
two directions, including children with parentally per-
ceived sleep problems while simultaneously excluding
severely sleep-disturbed individuals.
There were no statistically significant differences
between the participants who remained in the study at T2
123
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and the drop-outs who only participated at T1 in regards to
the seven measures of sleep analysed in this paper with the
exception for sleep efficiency which was somewhat lower
in the drop-outs. Thus, it is possible that some participants
with more sleep disturbances were not included at the T2.
Moreover, at follow-up all available children were retained
in the study, for example children with allergic complaints,
and in one case, a child with diabetes type 1, and also a few
children with pharmacological treatment.
Another limitation could be that the possibility of daytime
napping as a confounding factor was not considered in the
analyses of night-time sleep. Although actigraphy measure-
ments collected at night are considered accurate, reliable
assessments of daytime sleep is difficult with actigraphy
within daily activities. Furthermore, other confounding fac-
tors for example differing school start times or pubertal
development were not assessed. All of these limitations
should be considered when interpreting the results, and the
findings need to be replicated using larger samples, as well as
within different cultural contexts (Jenni and O’Connor 2005).
To conclude, the present actigraphic study indicates that
the change of essential aspects of sleep patterns is quite
similar in children with AS/HFA and in typically devel-
oping children over a 2 to 3-year period. Out of differences
in sleep timing, initiation, and maintenance observed at
baseline merely a difference in sleep maintenance was
persistent at follow-up.
Acknowledgment Development of this paper was supported with
funding from the Foundation of Majblommans Riksförbund.
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