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Sleep Medicine 9 (2007) 64–70

www.elsevier.com/locate/sleep

Original Article

Sleep in children with autistic spectrum disorder: A questionnaire


and polysomnographic study
Silvia Miano a, Oliviero Bruni b, Maurizio Elia a, Alessia Trovato a, Arianna Smerieri c,
Elisabetta Verrillo b, Michele Roccella d, Mario G. Terzano c, Raffaele Ferri a,*
a
Department of Neurology, Sleep Research Centre, Oasi Institute for Research on Mental Retardation and Brain Aging (IRCCS),
Via C. Ruggero 73, 94018 Troina, Italy
b
Department of Developmental Neurology and Psychiatry, Center for Pediatric Sleep Disorders, University ‘‘La Sapienza’’, Rome, Italy
c
Department of Neurology, Sleep Disorders Center, University of Parma, Italy
d
Department of Psychology, University of Palermo, Palermo, Italy

Received 22 November 2006; received in revised form 29 January 2007; accepted 31 January 2007
Available online 28 August 2007

Abstract

Objective: To evaluate sleep in children with autistic spectrum disorder (ASD) by means of sleep questionnaires and polysomnog-
raphy; moreover, to analyze their cyclic alternating pattern (CAP).
Methods: Thirty-one patients with ASD (28 males, 3 females, aged 3.7–19 years) and age-matched normal controls were included.
ASD children were evaluated by a standard sleep questionnaire that consisted of 45 items in a Likert-type scale covering several
areas of sleep disorders and by overnight polysomnography in the sleep laboratory after one adaptation night.
Results: The questionnaire results showed that parents of ASD children reported a high prevalence of disorders of initiating and
maintaining sleep, enuresis, repetitive behavior when falling asleep, and daytime sleepiness. Polysomnographically, ASD children
showed reduced time in bed, total sleep time, sleep period time and rapid eye movement (REM) latency. ASD subjects had a
CAP rate during slow-wave sleep (SWS) lower than normal controls, together with a lower percentage of A1 subtypes.
Conclusions: ASD children questionnaires showed a higher percentage of disorders of initiating and maintaining sleep than normal
controls; this was not completely confirmed by sleep staging. CAP measures showed subtle alterations of NREM sleep which could
be detected with an appropriate methodology of analysis. The reduction of A1 subtypes during SWS might play a role in the impair-
ment of cognitive functioning in these subjects.
Ó 2007 Elsevier B.V. All rights reserved.

Keywords: Autistic spectrum disorder; Sleep questionnaire; Actigraphy; Polysomnography; Sleep stages; Cyclic alternating pattern

1. Introduction fore, the study of sleep patterns in subjects affected by


specific types of mental retardation has been suggested
Sleep disturbances have frequently been reported in in order to avoid generalization on results that might
children with intellectual disabilities [1–3]. Several stud- not be clinically useful [3].
ies have shown that sleep problems in children with In children with autistic spectrum disorder (ASD),
mental retardation are frequently related to the specific questionnaire studies have shown a high rate of sleep
type of syndrome or to its etiological factors [4]; there- problems with respect to other groups of children who
have intellectual disabilities [5–7]. Parents of ASD chil-
*
Corresponding author. Tel.: +39 0935 936111; fax: +39 0935
dren report a prevalence of sleep problems ranging from
936694. 44% to 83% [8], mainly represented by difficulty falling
E-mail address: rferri@oasi.en.it (R. Ferri). asleep, restless sleep, frequent awakenings and reduced

1389-9457/$ - see front matter Ó 2007 Elsevier B.V. All rights reserved.
doi:10.1016/j.sleep.2007.01.014
S. Miano et al. / Sleep Medicine 9 (2007) 64–70 65

total sleep time during the night [8]. These sleep distur- the study were obese and the parents did not report
bances have been hypothesized to have a predictive role snoring in the children at the time of the study. Intelli-
in autistic behavior during the day [9]. gence level was measured by the Weschler Intelligence
On the other hand, polysomnographic (PSG) studies Scale for Children Revised [22] or by the Weschsler
showed only a reduced total sleep time [10–12] as the Adult Intelligence Scale [23] when appropriate for age.
main feature of sleep architecture in autism. Seventeen children had severe mental retardation (corre-
An attempt to classify sleep architecture in autism sponding to I.Q. in the range 25–40) and four had mod-
defined three types of sleep patterns [13]: (1) immaturity erate mental retardation (I.Q. in the range 40–55);
of sleep with disrupted PSG architecture, (2) functional mental retardation was not specified in nine of the chil-
alterations of sleep with early waking and bedtime resis- dren. Informed consent was obtained by the parents of
tance, (3) paroxysmal alterations with epileptiform dis- all participants in the study. All children were living at
charges, not necessarily occurring together with seizures. home.
Few studies tried to analyze sleep structure in order
to characterize better sleep of autistic children. Diomedi 2.2. Questionnaire study
et al. [14] found a higher density of spindle activity not
only during sleep stage 2 non-rapid eye movement A questionnaire arranged for the study of sleep char-
(NREM) sleep but also during slow-wave sleep (SWS) acteristics of children and adolescents [16,17] was filled
and rapid eye movement (REM) sleep; during REM out by the parents. The sleep questionnaire consisted
sleep, other authors found a higher density of muscle of 45 items in a Likert-type scale with values 1–5
twitches [10] that seems to be related to pontine-tegmen- (1 = never; 2 = occasionally; 3 = often; 4 = very often;
tum alterations [15] and briefer bouts of rapid eye move- 5 = always) to measure individual differences in several
ments [11]. areas of sleep disorders (e.g., disorders of initiating
The aim of this study was to collect data from a stan- and maintaining sleep, sleep–wake transition disorders,
dard sleep questionnaire [16,17] and to perform PSG other parasomnias, night waking, movement disorders
recordings analyzing traditional sleep architecture and during sleep, breathing problems during sleep, excessive
the cyclic alternating pattern (CAP) [18,19], in order to daytime somnolence and morning symptoms). Some
obtain additional information on NREM sleep micro- items were removed from the original questionnaire
structure in these patients. because the clinical features of ASD children, language
capabilities in particular, did not allow their parents to
2. Methods evaluate some disorders (waking up complaining of
headache, waking up with leg cramps, report of fright-
2.1. ASD Subjects ening dream, hypnagogic hallucinations and hallucina-
tions upon waking up in the morning). The
A total of 31 children attending the Oasi Institute of questionnaire assessed sleep behaviors and disorders
Troina and who were affected by ASD (28 males, 3 observed during the last six months of the subject’s life.
females, age range 3.7–19 years, mean age 9.53 years, All 31 ASD subjects participated in this study and the
SD, 3.82) were recruited for this study. The diagnosis mothers of all the ASD children filled out the question-
of autism was made according to Diagnostic and Statis- naire. The control group was composed of a large
tical Manual of Mental Disorders, Fourth edition cohort of normal healthy Caucasian children and ado-
(DSM-IV) [20] criteria for autistic disorder and a score lescents, mostly from families with a working and mid-
on the Childhood Autism Rating Scale [21] >30. All dle class background, randomly selected in three
patients were also mentally retarded and drug-free for public schools of Rome (442 males and 451 females,
at least two weeks before the study began. All subjects mean age 9.9 years; range 6.5–14.10). Family factors
were evaluated from the neuroimaging (including were similar for both groups (patients and controls)
brain-computed tomography scans or magnetic reso- and the education level of mothers and fathers did not
nance imaging) and the neurophysiological (electroen- differ significantly for the two groups.
cephalography [EEG]) points of view and showed no
neurological focal signs, seizures or paroxysmal EEG 2.3. Polysomnographic (PSG) study
abnormalities. This allowed us to rule out the possibility
of gross neurological impairment. No other known med- For this study, ASD subjects whose parents agreed to
ical conditions were associated with autism in these participate and who were collaborative underwent an
patients and, specifically, those with craniofacial abnor- overnight PSG recording in the Sleep Laboratory of
malities, fragile-X syndrome or other chromosome the Oasi Institute of Troina, after one adaptation night
abnormalities, such as phenylketonuria or other meta- in order to avoid the first-night effect. We excluded
bolic diseases, neurofibromatosis or tuberous sclerosis patients whose parents reported respiratory sleep distur-
were excluded. None of the ASD subjects included in bances or abnormal sleep patterns on the questionnaire.
66 S. Miano et al. / Sleep Medicine 9 (2007) 64–70

The sample was, therefore, composed of 16 males (mean the end of the second B-phase and the third A-phase is
age 9.4 years; standard deviation (SD), 2.33). The PSG quantified as non-CAP. This is because the CAP proce-
data were compared with those of a control group dure is based on the succession of complete CAP cycles
formed by 18 children matched for age (9 females and (phase A + phase B).
9 males, mean age 10.2 years; SD, 2.93). CAP A phases have been subdivided into a three-
The PSG montage included at least three EEG chan- stage hierarchy of arousal strength:
nels (including C3 and C4, in particular) referenced to
the contralateral mastoid, left and right electrooculo- - A1: A phases with synchronized EEG patterns (inter-
gram (EOG) referred to the contralateral mastoid, chin mittent a rhythm in S1; sequences of K-complexes or
electromyogram (EMG), and electrocardiogram (ECG). d bursts in the other NREM stages), associated with
All recordings started at the patients’ usual bedtime and mild or trivial polygraphic variations;
continued until spontaneous awakening. - A2: A phases with desynchronized EEG patterns
preceded by or mixed with slow high-voltage waves
2.4. Sleep architecture (K-complexes with a and b activities, k-a, arousals
with slow-wave synchronization), linked with a mod-
In all subjects, sleep was subdivided into 30-s epochs erate increase of muscle tone and/or cardiorespiratory
and sleep stages were scored according to the standard rate;
criteria by Rechtschaffen and Kales [24]. - A3: A phases with desynchronized EEG patterns
The following conventional sleep parameters were alone (transient activation phases or arousals) or
evaluated: exceeding 2/3 of the phase A length, and coupled with
a remarkable enhancement of muscle tone and/or car-
- Time in bed (TIB); diorespiratory rate.
- Sleep period time (SPT): time from sleep onset to
sleep end; The following CAP parameters were measured:
- Total sleep time (TST): the time from sleep onset to
the end of the final sleep epoch minus time awake; - CAP rate (percentage of total NREM sleep time
- Sleep latency (SL): time from lights out to sleep onset, occupied by CAP sequences);
defined as the first of two consecutive epochs of sleep - Percentage and duration of each A phase subtype;
stage 1 or one epoch of any other stage, in minutes; - A1 index (number of phases A1 per hour of NREM
- REM latency (RL): time from sleep onset to the first sleep, and of S1, S2 and SWS sleep stage);
REM sleep epoch; - A2 index (number of phases A2 per hour of NREM
- Number of stage shifts/hour (SS/h); sleep, and of S1, S2 and SWS sleep stage);
- Number of awakenings/hour (AWN/h); - A3 index (number of phases A3 per hour of NREM
- Sleep efficiency (SE%): the percentage ratio between sleep, and of S1, S2 and SWS sleep stage);
total sleep time and time in bed (TST/TIB * 100); - Duration of B phases;
- Percentage of SPT spent in wakefulness after sleep - Number and duration of CAP sequences.
onset (WASO%) (i.e., the time spent awake between
sleep onset and end of sleep); All these variables were analyzed by means of the
- Percentage of SPT spent in sleep stages 1 (S1%), 2 Hypnolab 1.2 sleep software analysis (SWS Soft, Italy).
(S2%), slow-wave sleep (SWS%), and REM sleep All the recordings were visually scored by one of the
(REM%). investigators (SM), and the sleep parameters derived
were tabulated for statistical analysis.

2.5. Cyclic alternating pattern (CAP) 2.6. Statistical analysis

CAP was scored following the criteria by Terzano The comparison between the ASD patient groups and
et al. [25]; CAP is periodic EEG activity of NREM sleep age-matched normal controls for the questionnaire data
characterized by repeated spontaneous sequences of was carried out by means of the non-parametric v2 test.
transient events (phase A), recurring at intervals up to For the PSG studies, comparison between sleep param-
2 min long. The return to background activity identifies eters obtained in normal controls and ASD children was
the interval that separates the repetitive elements (phase conducted using the nonparametric Mann–Whitney test
B). In particular, phase-A candidates are scored within a for independent data sets. Differences were considered
CAP sequence only if they precede and/or are followed statistically significant at p < 0.05. The commercially
by another phase A in the temporal range of 2–60 s. If available software STATISTICA (data analysis soft-
there are three consecutive A-phases followed by a ware system), version 6, StatSoft Inc. (2001) was used
non-CAP condition, the CAP sequence is stopped at for all statistical tests.
S. Miano et al. / Sleep Medicine 9 (2007) 64–70 67

3. Results (b) Bedtime problems. ASD patients showed a higher


prevalence of bedtime problems, mainly repre-
3.1. Sleep questionnaire sented by difficulty getting to sleep at night
(25.81% vs. 8.86%) and also 19.35% of ASD sub-
Table 1 reports the results of the questionnaire study. jects needed to take fluids or drugs in order to fall
Parental reports showed that ASD children had a higher asleep versus 0.67% of the control group;
prevalence of several sleep disorders: (c) Sleep–wake transition disorders. Hypnic startles
and rhythmic movement disorders were more pre-
(a) Sleep duration and sleep latency. ASD patients valent in ASD subjects;
showed a sleep duration lower than 8 h in (d) Night awakenings. ASD children showed a more
22.58% versus 9.63% of the control group; in interrupted sleep since they had more than two
addition, sleep latency was prolonged with awakenings per night in 16.13% versus 6.83% of
25.81% of ASD subjects who took more than the control group and complained of difficulty fall-
30 min to fall asleep versus 6.61% in the control ing asleep again after awakenings (25.81% vs.
group; 4.82%);

Table 1
Questionnaire item responses in ASD subjects and normal controls
Questionnaire items Normal controls (n = 893) (%) ASD patients (n = 31) (%) v2 p<
1. Sleeps less than 8 h 9.63 22.58 5.55 0.02
2. Latency to sleep > 30 min 6.61 25.81 16.42 0.00001
3. Reluctant to go to bed 29.68 29.03 0.01 NS
4. Bedtime variations 38.6 38.71 0.00 NS
5. Difficulty getting to sleep at night 8.86 25.81 9.87 0.002
6. Anxiety/fear when falling asleep 8.17 12.90 0.88 NS
7. Drinks stimulant beverages in the evening 27.32 6.45 63.12 0.00001
8. Need for light or TV in the bedroom 27.21 22.58 0.33 NS
9. Need for a transitional object 18.2 25.81 1.13 NS
10. Fluids or drugs to facilitate sleep 0.67 19.35 81.58 0.00001
11. Hypnic jerks 5.04 35.48 48.78 0.00001
12. Rhythmic movements while falling asleep 2.69 16.13 17.81 0.00001
13. Falling asleep sweating 10.30 16.13 1.08 NS
14. Poor sleep quality 13.89 87.10 117.46 0.00001
15. More than two awakenings per night 6.83 16.13 3.91 0.05
16. Waking up screaming in the night 5.49 0.00 1.80 NS
17. Waking up to drink or eat in the night 13.55 29.03 5.94 0.015
18. Getting up to use to the bathroom 10.64 3.23 1.77 NS
19. Difficulty to fall asleep after awakenings 4.82 25.81 25.31 0.00001
20. Nocturnal hyperkinesias 29.00 25.81 0.15 NS
21. Unusual movements during sleep 5.94 0.00 1.95 NS
22. Pains of unknown origin during sleep 0.56 3.23 3.30 NS
23. Convulsions during sleep 0.67 0.00 0.21 NS
24. Sleep breathing difficulties 6.83 9.68 0.38 NS
25. Sleep apnea 1.01 0.00 0.32 NS
26. Snoring 14.67 16.13 0.05 NS
27. Night sweating 15.90 12.90 0.20 NS
28. Sleep walking 3.14 3.23 0.00 NS
29. Sleep talking 14.45 6.45 1.57 NS
30. Bedwetting 2.35 22.58 41.72 0.00001
31. Bruxism 7.39 16.13 3.22 NS
32. Sleep terrors 1.34 0.00 0.42 NS
33. Nightmares 2.46 0.00 0.78 NS
34. Difficulty in waking up in the morning 35.95 29.03 0.62 NS
35. Variation of waking time 25.87 35.48 1.43 NS
36. Sleep paralysis 4.14 6.45 0.39 NS
37. Daytime somnolence 4.48 12.90 4.69 0.03
38. Falling asleep at school 0.34 3.23 5.80 0.02
39. Sleep attacks 1.46 3.23 0.63 NS
68 S. Miano et al. / Sleep Medicine 9 (2007) 64–70

(e) Parasomnias. ASD children showed a higher prev- 3.2. Polysomnography (PSG)
alence of bedwetting compared to controls
(22.58% vs. 2.35%); (a) Sleep architecture. Table 2 shows the statistical
(f) Morning symptoms and daytime sleepiness. Diurnal comparison between the sleep architecture param-
somnolence affected 12.90% of ASD children (vs. eters obtained from the ASD patients and the con-
4.48% of controls), and it is possible that this som- trol group: ASD children had a reduced time in
nolence was also responsible for falling asleep at bed associated with a reduced total sleep time
school (3.23% vs. 1.46%). and total sleep duration. They also showed a
shorter REM latency compared to controls.

Table 2
Polysomnographic sleep architecture parameters found in ASD children and normal controls
Normal controls (n = 18) ASD patients (n = 16) Mann–Whitney U-test
Mean SD Mean SD p<
TIB (min) 534.3 52.98 492.9 36.23 0.044
SPT (min) 505.5 47.65 453.9 53.94 0.014
TST (min) 493 46.87 438.5 54.94 0.007
SL (min) 22.9 14.58 37.5 42.18 NS
RL (min) 114.6 37.16 84.3 39.27 0.02
SS (h-1) 5.1 1.54 5.8 1.28 NS
AWN (h-1) 0.5 0.54 0.9 0.71 NS
SE (%) 92.5 5.37 89.0 8.67 NS
WASO (%) 2.4 3 3.3 5.31 NS
S1 (%) 4 4.31 5.8 7.35 NS
S2 (%) 47.1 5.47 43.2 10.88 NS
SWS (%) 23.3 5.48 25.9 10.38 NS
REM (%) 23.3 5.1 21.9 3.95 NS
TIB, time in bed; SPT, sleep period time; TST, total sleep time; SL, sleep latency; RL, REM latency; SS, stage shifts; AWN, awakenings number; SE,
sleep efficiency; WASO, wakefulness after sleep onset; S1, stage 1; S2, stage 2; SWS, slow wave sleep; REM, REM sleep.

Table 3
CAP parameters found in ASD children and normal controls
Normal controls (n = 18) ASD patients (n = 16) Mann–WhitneyU-test
Mean SD Mean SD p<
Total CAP rate (%) 37.9 7.27 36.8 10.39 NS
In S1 (%) 33.5 21.48 39.4 18.64 NS
In S2 (%) 33.9 10.77 40.4 13.68 NS
In SWS (%) 47.3 8.67 33.9 15.47 0.02
A1 (%) 77.9 8.43 65.1 8.35 0.0004
A2 (%) 12.8 7.03 19.7 6.23 0.006
A3 (%) 9.4 3.02 15.1 6.16 0.002
A1 duration (s) 4.8 0.33 4.9 0.32 NS
A2 duration (s) 7.8 1.75 6.6 0.79 0.04
A3 duration (s) 15.3 4.83 12.5 1.51 NS
A1 index 47.0 10.67 38.2 10.12 0.04
In S1 33.2 20.93 25.5 20.49 NS
In S2 43.8 10.81 41.4 13.45 NS
In SWS 77.7 18.94 52.6 22.58 0.004
A2 index 8.7 6.38 12.3 6.52 NS
In S1 6.4 6.31 8.5 8.05 NS
In S2 11.2 8.15 19.3 9.65 0.02
In SWS 6.8 4.55 5.0 3.25 NS
A3 index 5.5 3.17 8.9 5.74 0.03
In S1 16.7 13.13 33.3 24.04 0.04
In S2 8.1 3.44 12.5 8.00 0.05
In SWS 2.6 1.72 4.6 3.85 NS
B duration (s) 20.7 4.14 19.5 2.30 NS
Sequence duration (s) 195.3 42.84 180.1 38.55 NS
No. of sequences 44.9 9.62 41.6 7.92 NS
CAP, cyclic alternating pattern; ASD, autistic spectrum disorder; SWS, slow wave sleep.
S. Miano et al. / Sleep Medicine 9 (2007) 64–70 69

(b) Cyclic alternating pattern (CAP). The assessment rate associated with a low A1 index during SWS and
of CAP (Table 3) revealed that subjects with increased A2 and A3 indexes during light sleep. The
ASD had a lower CAP rate during SWS than increase of A2 and A3 subtypes during light sleep might
did normal controls. Moreover, ASD patients counterbalance the reduction of A1 phases during SWS,
showed a lower percentage of A1 subtypes, with and this might explain the fact that the total CAP rate
a higher percentage of A2 and A3 subtypes com- showed no differences between the two groups. As
pared to controls, as well as reduced A1 index already seen for other neurophysiological parameters,
and increased A3 and A2 indexes. In particular, PSG features of autistic mentally retarded subjects also
there was a significant reduction of A1 index only seem to show only subtle alterations which can be
in SWS, accompanied by an increase of A2 index detected with an appropriate methodology capable of
during sleep stage 2 and of the A3 index during picking up small (but significant) changes, such as CAP.
sleep stages 1 and 2. Furthermore, the duration The increase in A2 and A3 index might be caused by
of A2 subtypes was shorter in children with ASD other sleep disorders that were not detected by the sim-
compared to controls. ple PSG recording we performed in the ASD group,
such as sleep-disordered breathing or periodic limb
movements disorders (PLMD), and the reduction of
4. Discussion the percentage of A1 subtypes and A1 index in SWS
seems to be a peculiar alteration of sleep in our ASD
To the best of our knowledge, this study represents sample.
the first attempt to evaluate thoroughly the sleep pat- The slow-wave activity during NREM sleep has been
terns of ASD children, taking into consideration sleep indicated as a crucial component of the recently hypoth-
architecture and microstructure by means of CAP esized synaptic downscaling during sleep, probably
analysis. important for cognitive processing [27–29]. The most
Some limitations of the study should be taken into important component of CAP is slow-wave activity
account. For example, although we did not include [30], with an important role in the generation of these
ASD children whose parents reported habitual snoring, slow waves played by the frontal brain regions [31]
respiratory sleep disturbances or abnormal sleep pat- and, probably, by transcallosal pathways interconnect-
terns and those with craniofacial abnormalities or with ing these regions [32]. Indeed, interaction between
obesity, we were not able to exclude polysomnographi- higher cognitive functions and the regulation of sleep
cally the presence of sleep respiratory disorders as we and affective functioning appears to be modulated by
did not record respiratory parameters. This was done the prefrontal cortex, which acts as the interface of the
in order to improve the compliance to the PSG sleep/arousal system, the affective system, and higher
recording. cognitive-neurobehavioral systems [33]. The significant
The questionnaire results showed that parents of decrease in A1 CAP subtypes might point to a possible
ASD children reported, in comparison to normal con- dysfunction of these brain structures in our ASD
trols, mainly a higher prevalence of disorders of initiat- patients, which might play a role in the impairment of
ing and maintaining sleep, enuresis and repetitive cognitive functioning in these subjects. Frontal lobe dys-
behavior when falling asleep; this seems to confirm the function has been also reported in autistic patients by
parental perception of sleep fragmentation in ASD, as means of other neurophysiological techniques [34,35].
reported by other studies [8]. The results of the question- Another clinical condition of childhood characterized
naire study were not completely confirmed by sleep by frontal lobe dysfunction is attention-deficit hyperac-
architecture analysis which showed a reduced total sleep tivity disorder (ADHD). We have previously performed
time but normal sleep latency. In fact, PSG data showed CAP analysis in ADHD children [36] and showed that
only few differences between ASD and normal children, their CAP is characterized by a low level of arousability
mainly a reduction of TIB, TST and SPT, in agreement (lower NREM CAP rate compared to normal controls)
with the findings of previous studies [10,12,14]. As and by a decrease of A1 index in stage 2 NREM.
already reported by Elia et al. [10], the reduction in The reduction of A1 in SWS in our ASD sample
TIB, SPT and TST values might be a consequence of might be peculiar of this disorder. Since our ASD group
the dysfunction of the brainstem aminergic (dopaminer- was composed of children affected by a moderate/severe
gic and serotonergic) pathways which has already been mental retardation, we can not establish whether this
demonstrated in ASD [26]. alteration of NREM CAP is a characteristic of ASD
From the sleep microstructure point of view, subtle or if it is a general feature of mentally retarded subjects.
alterations of the arousal level fluctuations during Future studies are needed to compare the CAP parame-
NREM sleep, measured by means of CAP, were found ters of ASD patients and matched groups of mentally
in the ASD group. CAP analysis showed in ASD sub- retarded subjects in order to characterize CAP in non-
jects, compared to normal controls, mainly a low CAP autistic mentally retarded subjects.
70 S. Miano et al. / Sleep Medicine 9 (2007) 64–70

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