Biological Psychiatry
Original Paper
Neuropsychobiology 2004;50:147–152
DOI: 10.1159/000079106
Sleep in Young Adults with
Asperger Syndrome
Pekka Tani a, c Nina Lindberg a, c Taina Nieminen-von Wendt b
Lennart von Wendt b Jussi Virkkala d Björn Appelberg a
Tarja Porkka-Heiskanen c
a Department of Psychiatry, Helsinki University, b Hospital for Children and Adolescents, Helsinki University
Central Hospital, c Institute of Biomedicine, Helsinki University, Helsinki, and d Clinical Neurophysiology Section,
Tampere University Hospital, Tampere, Finland
Key Words
Asperger syndrome W Sleep W Polysomnography
Abstract
Asperger syndrome (AS) is a neurodevelopmental disor-
der belonging to autism spectrum disorders. Both chil-
dren and adults with AS have subjective impairment in
the initiation and continuity of sleep, and studies using
objective assessment are sparse. Twenty young AS
adults with frequent complaints of low sleep quality
were compared to 10 age-, gender- and education-
matched controls without sleep complaints using poly-
somnography and spectral power analysis of slow-wave
sleep. AS subjects displayed a similar polysomno-
graphic profile as compared with controls. In spectral
power analysis, a statistically nonsignificant trend to-
wards decreased relative delta power and increased the-
ta power in slow-wave sleep was found in the AS group.
It seems that nonorganic insomnia, due to anxiety inher-
ent in AS, is responsible for the low sleep quality in these
subjects.
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Introduction
Asperger syndrome (AS) is a pervasive developmental
disorder characterized by altered social interactions, re-
stricted interests and repetitive and stereotyped behavior
as in autism, but, contrary to the latter, should not show
any significant delay in the acquisition of language, psy-
chomotor and cognitive skills [1]. According to epidemio-
logical surveys, AS is not uncommon, the prevalence
being 0.35% in school-age children [2]. The prevalence of
AS in adulthood is unknown, but, as AS is a continuous
and lifelong disorder [1], it is reasonable to assume that it
is not significantly lower than in childhood. Most studies
on AS concentrate on childhood, while there is scarcity of
reports about the clinical and neurobiological characteris-
tics of these individuals in adulthood.
Autism, AS and pervasive developmental disorder not
otherwise specified are commonly referred to as ‘autistic
spectrum disorders’ (ASD) [3]. In children with ASD, the
initiation and continuity of sleep is disturbed to a greater
degree than in children with other developmental disor-
ders [4]. More specifically, in a sleep questionnaire study
concerning sleep problems in AS children, they differed
Pekka Tani, MD
Institute of Biomedicine, Department of Physiology
University of Helsinki, Haartmaninkatu 8
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from age-matched controls in respect of the high degree of
dyssomnias, especially in the difficulty in initiating and
maintaining sleep [5].
A polysomnographic study on children and adoles-
cents with autism disclosed significantly shorter sleep
periods (SP), total sleep time (TST) and time in bed (TIB)
compared with controls [6]. In another study using poly-
somnography in AS patients of different ages from child-
hood to middle age, no significant differences were found
in TST and sleep efficiency (SE%) in comparison with
controls [7].
We have reported a high prevalence of insomnia in AS
adults assessed with a sleep questionnaire [8] and sleep
diary [9]. The experience of insomnia may be associated
with objective alteration of sleep architecture or, alterna-
tively, with deviant perception of sleep due to psychologi-
cal factors [10]. Thus, the possible clinical implications
warrant further study of sleep quality with more objective
methods. There seems to be decreased delta power and
increased beta power in non-REM sleep of adults with
subjective insomnia [11] and therefore, in the present
study, slow-wave sleep (SWS) was chosen as a target for
spectral power analysis.
The aim of the present study was to characterize the
quality of sleep in young adults with AS using two of the
most objective measures of sleep, polysomnography and
spectral power analysis of sleep. The hypothesis was that
AS adults do not differ from controls regarding polysom-
nographic sleep, but that they display heightened arousal
in SWS because of insomnia.
Materials and Methods
Subjects
Diagnosis of AS
AS subjects (n = 20, mean age B SD 27.2 B 7.3 years) were, after
having given their informed consent, recruited from the Helsinki
Asperger Center, a unit to which patients with a tentative diagnosis
of AS are referred from all parts of Finland. The diagnosis of AS was
a carefully assessed lifetime best estimate using multiple sources of
information [8].
The detailed clinical characteristics of AS subjects and controls
have previously been published [8, 9]. None of the participants had
neurological or metabolic diseases that might confound polysomno-
graphic assessment. In sleep diary, most of the AS subjects had a
variable degree of insomnia without sleep deprivation or circadian
rhythm disorder.
Thirteen AS subjects met the diagnostic criteria of one or more
anxiety disorders, the most prevalent being social phobia (n = 8).
Five AS subjects had mild to moderate depressive disorder and none
of them had severe major depressive disorder. Obsessive-compulsive
personality disorder (12 subjects) or traits of it (7 subjects) were the
148 Neuropsychobiology 2004;50:147–152
most common axis II disorders. Four AS subjects were devoid of any
other axis I or axis II disorders besides AS. Subjects with schizophre-
nia or other chronic psychotic illness noted in previous medical rec-
ords or in the Structured Clinical Interview for DSM-III-R were
excluded from the present study because these disorders are known
to have a profound effect on polysomnographic parameters of sleep
[12]. None of the participants had a diagnosis of alcohol misuse or
dependency.
In the sleep questionnaire, 2 AS subjects and 1 control reported
snoring at least 1–2 nights per week and none of the participants had
breathing pauses during sleep (information also from significant oth-
ers) [9]. Two AS subjects and none of the controls had symptoms of
restless legs syndrome according to standardized criteria [13].
During the study period, 3 AS subjects and 1 control smoked 5
cigarettes or more per day. Three AS subjects and 1 control had
drunk more than 24 g alcohol per evening on 1 or 2 nights, but not in
the nights preceding polysomnography. One AS subject and 1 control
reported excessive use of coffee (more than 3 cups per day).
Participants were medication free (with a minimum interval of
2 weeks for hypnotics, 3 months for antidepressant medicines and
1 year for neuroleptics).
Control Group
The control group (n = 10), consisting of volunteers, had no
anamnesis of neuropsychiatric disorders, no current axis I or axis II
psychiatric disorders and no complaints of sleep problems. Thirty
percent of the participants were women both in the AS group and in
controls. In both groups, 80% of the participants had education at
college level or above. Age in the AS group (mean B SD 27.2 B 7.3
years) did not differ from that of the controls (mean B SD 26.5 B 8.1
years). Total IQ assessed with the Wechsler Adult Intelligence Scale-
Revised was the same in the AS group (mean B SD 111.6 B 11.9)
and in controls (mean B SD 111.2 B 10.4) and all participants were
in the range of normal intelligence.
Sleep Assessment
Polysomnography was performed in 2 consecutive nights for each
participant. Results of the second night recordings were included in
the analysis. The recording took place in a guest room in Lapinlahti
hospital on ambulatory basis; participants had a portable recording
device (Embla, Flaga hf, Reykjavik, Iceland) that was connected to
the recording electrodes. They were advised to push the event button
when they went to bed in the evening. They lived their ordinary life
and only came to the hospital in the evening for the attachment of the
recording system and left the hospital in the following morning.
C3-A1 and C4-A1 channels recorded EEG activity, EOG elec-
trodes were placed according to standard criteria [14] and EMG was
recorded submentally.
Sleep stages were scored from the C4-A1 channel by an experi-
enced polysomnographist (S.P.) blinded to the clinical information,
in 30-second epochs, according to standard criteria. High-pass filter
was 0.5 Hz and low-pass filter 45 Hz, with a sampling rate of 100 Hz.
A commercial software (Somnologica, Version 2.0, Flaga hf) was
used for the scoring and calculation of sleep parameters. Sleep onset
was defined as the first occurrence of three consecutive epochs (90 s)
of sleep. Sleep spindles were calculated with automatic analysis of
Somnologica 3.1.3 (Medcare, Reykjavik, Iceland) with default set-
tings using the C4-A1 channel.
The following parameters were calculated: TIB, sleep latency
(Lat), SP (SP = TIB – Lat), TST (TST = SP – WASO), wake after
Tani et al.
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sleep onset (WASO), SE% (SE% = TST/SP), number of awakenings, Table 1. Polysomnographic data of 20 subjects with AS and 10 con-
number of sleep spindles/sleep stage 2 (S2) min, S1 – S4% (of TST), trols
and REM% (of TST). REM latency was calculated from sleep onset.
Power spectrum was calculated from the C4-A1 channel, for each AS Controls T (d.f.) p
30-second epoch using 512-point fast Fourier transformation, with
50% overlapping and Hanning window, in five frequency bins (band TIB1, min 533B16 511B18 0.845 (28) n.s.
widths: delta: 0.5–3.5 Hz, theta: 3.5–8.0 Hz, alpha: 8.0–12.0 Hz, sig- Sleep latency2, min 31B7 22B9 T = 130.0 n.s.
ma: 12.0–14.5 Hz and beta: 14.5–25.0 Hz), separately for S2 and Sleep period1, min 501B18 489B19 0.426 (28) n.s.
SWS (S3 + S4). The spectral powers in all frequency bins were nor- TST1, min 441B21 457B18 –0.497 (28) n.s.
malized in each recording to the total power in S2 and SWS to enable WASO2, min 61B15 32B12 T = 120.0 n.s.
comparisons between persons. SE%2 88.0B2.7 93.8B2.2 T = 189.5 n.s.
Awakenings 21B3 19B2 0.473 (28) n.s.
Ethics S1%1, 3 11.9B1.0 10.0B1.0 1.167 (28) n.s.
Informed consent was obtained from all participants. The study S2%1, 3 50.9B1.3 55.6B2.7 –1.749 (28) n.s.
was approved by the local ethical committee and principles of the SWS%1, 3 14.5B2.0 9.7B2.6 1.417 (28) n.s.
declaration of Helsinki were adequately followed. REM%1, 3 22.7B1.3 24.7B1.3 –0.944 (28) n.s.
REM latency2, min 105B17 81B11 T = 147.5 n.s.
Statistics
Polysomnographic and power spectrum parameters of sleep were Results are means B SEM. n.s. = No statistically significant dif-
compared between AS subjects and controls using Student’s t test or, ference between groups.
in case the parameter studied disclosed a nonnormal distribution, the 1 Student’s t test (two-tailed).
Mann-Whitney rank sum test was applied. Dichotomized differences 2 Mann-Whitney rank sum test.
within and between AS subjects and controls were calculated using 3 Percent of TST.
the Fisher exact test.

Results

In table 1, the polysomnographic variables of sleep in Table 2. Polysomnographic data of 20 subjects with AS and 10 con-
AS subjects compared with controls are displayed. The trols in the first half of the SP
distribution of sleep stages within the night was further
AS Controls T (d.f.) p
studied by splitting the SP into two halves. In table 2, the
polysomnographic data of the first half of the SP are dis- SE%2 87B5 96B2 T = 170 n.s.
played. AS subjects showed a similar polysomnographic WASO2, min 33B13 10B4 T = 134 n.s.
structure of sleep to controls, both in the first half and in Awakenings1 8B1 7B1 t = 0.076 (28) n.s.
S1%2 12B2 8B1 T = 131 n.s.
the entire SP. In the first half of the SP, both AS subjects
S2%1 51B2 56B4 t = –1.236 (28) n.s.
and controls had more SWS and less REM sleep, as com- SWS%1 21B3 17B4 t = 0.983 (28) n.s.
pared with the entire SP. Two AS subjects had an REM%1 16B2 19B2 t = –1.259 (28) n.s.
extremely long period of WASO in the first half of the SP
(145 and 226 min, respectively) and in the entire SP (149 Results are means B SEM. n.s. = No statistically significant dif-
and 275 min, respectively), leading to a nonnormal distri- ference between groups.
1 Student’s t test (two-tailed).
bution of WASO and SE%. 2 Mann-Whitney rank sum test.
The number of sleep transitions in the whole-night
polysomnography was calculated for the following param-
eters in 20 AS subjects and in 10 controls: all transitions,
all-wake, and transitions between REM sleep and any oth-
er sleep stages with no significant differences between
groups, even after correcting the results with the duration groups, shown in table 3. The larger proportion of AS sub-
of the SP in each participant. jects with WASO 630 min was the only distinguishing
Spindle frequency in relation to the amount of S2 sleep feature as compared with controls.
was equal in AS subjects compared with controls calcu- When the 6 women were compared to the 14 men (with
lated from the C4-A1 derivation. the t test) in the AS group, no significant difference was
Sleep quality was further studied by comparing the fre- found in age, the Beck Depression Inventory, and in all-
quency distribution of dichotomized differences between night polysomnographic parameters of sleep.

Sleep in Young Adults with Asperger Neuropsychobiology 2004;50:147–152 149

Syndrome
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Table 3. Dichotomized differences of polysomnographic sleep be- Discussion
tween 20 AS subjects and 10 controls
The main finding of the present study was that AS
AS Controls p
adults with frequent insomnia had a similar polysomno-
Total SP graphic and power spectrum pattern of sleep as compared
Latency 630 min, % 35 20 n.s. with controls devoid of sleep complaints.
TST ^390 min, % 30 10 n.s. Distribution of sleep stages within the SP was equal
SE% ^85%, % 30 20 n.s.
(and normal) both in AS subjects and in controls with a
WASO 630 min, % 65 20 0.05
WASO 660 min, % 35 20 n.s. greater amount of SWS (and a lesser amount of REM
REM latency ^90 min, % 70 70 n.s. sleep) in the early part of the SP. This is in accordance
with the preliminary finding of normal homeostatic sleep
First half of SP
SE% ! 85%, % 25 0 n.s. regulation in adults with ASD [15].
WASO 1 30 min, % 25 10 n.s. The only sign indicating decreased sleep continuity in
WASO 1 60 min, % 15 0 n.s the present study was the greater proportion of AS sub-
jects with WASO 130 min during the entire SP (table 3),
n.s. = No statistically significant difference between groups. The
which might be due to the 2 AS subjects with very long
Fisher exact test was used.
WASO.
Not surprisingly, the comorbid psychiatric diagnoses
of AS subjects consisted mainly of anxiety disorders, the
most prevalent being social phobia in 8 out of 13 subjects.
Table 4. Relative power spectrum from the C4-A1 channel in 20 AS Anxiety disorders tend, in general, to have a minimal
subjects and in 10 controls impact on polysomnography, while the subjective experi-
ence of difficulty in the initiation and continuity of sleep
AS Control t (d.f.) p
is more pronounced [16]. Social phobia is not associated
Whole night with polysomnographic changes in sleep quality [17],
S2 delta 67B1 69B2 t = 0.825 (27) n.s. while in the sleep questionnaire, persons with social pho-
S2 theta 19B1 17B1 t = 1.413 (27) n.s. bia display poor sleep quality, long Lat, more disturbed
S2 beta 2.4B0.2 2.2B0.2 t = 0.407 (27) n.s.
sleep and greater daytime dysfunction but equal duration
S3+4 delta 85B1 88B0.1 t = 1.775 (27) 0.09
S3+4 theta 10B1 9B1 t = 1.830 (27) 0.08 of sleep compared with controls [18], resembling the find-
S3+4 beta 0.7B0.1 0.5B0.1 t = 1.586 (27) n.s. ings in adult AS [9]. All AS subjects displayed one or mul-
tiple clinical anxiety symptoms, although in 65% these
First part of SP
S2 delta 68B2 72B2 t = 1.557 (27) n.s. reached the threshold of some clinical anxiety syndrome.
S2 theta 19B1 16B1 t = 1.984 (27) 0.06 Clinicians with substantial experience of AS have noticed
S2 beta 2.3B0.2 1.9B0.2 t = 1.084 (27) n.s. that pervasive anxiety is typical for adolescents and adults
S3+4 delta 84B1 88B1 t = 1.952 (26) 0.06 with AS [19] and might even be exaggerated in adults who
S3+4 theta 11B1 9B1 t = 1.990 (26) 0.06
have to cope with social settings at work or studies [20]. In
S3+4 beta1 0.8B0.1 0.5B0.1 T = 116 n.s.
the Temperament and Character Inventory, AS adults
Results are means B SEM. p ! 0.10 as a sign of trend are shown. score high on harm avoidance and low on self-directed-
n.s. = No statistically significant difference between groups. ness and novelty seeking [21], resulting in an anxiety-
1 Mann-Whitney rank sum test. prone, socially detached character with reluctance to ac-
cept changes.
On axis II, 19 AS subjects had obsessive-compulsive
personality disorder or traits of it. Similarity of obsessive-
compulsive personality disorder to AS, at least on the
In the all-night power spectrum of S2 and SWS, respec- symptom level, has previously been noted [22]. In a study
tively, no difference was found between AS subjects and where 100 patients with chronic insomnia were assessed
controls (table 4). However, a consistent tendency (p ! with a structured psychiatric interview, 95% of the subjects
0.10) towards lower relative delta power and higher theta had multiple psychiatric diagnoses, the most prevalent
power in SWS was found in the AS group as compared being anxiety disorders and dysthymia as well as substance
with controls. use disorders on axis I, and obsessive-compulsive person-

150 Neuropsychobiology 2004;50:147–152 Tani et al.

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ality disorder or traits of it on axis II [23]. Our findings are
grossly in agreement with this study, except that sub-
stance use disorders were lacking in the present sample.
Alexithymia characterizes AS adults [8] as well as
patients with panic disorder and social phobia [24]. Inter-
estingly, the factor analysis of different facets of alexithy-
mia produced similar findings both in AS subjects and in
patients with anxiety disorders. In a population study,
functional insomnia associates with alexithymic features
[25]. On the other hand, alexithymic traits per se are not
associated with objective abnormalities of sleep [26].
We are not aware of previous studies of sleep in ASD
where spectral power analysis would have been included.
The EEG spectral power analysis is used to provide more
accurate information about sleep than traditional poly-
somnography; while the sleep scoring is based on a subjec-
tive evaluation of the recording, spectral power analysis is
fully computerized. In the present study, spectral power
analysis in fact confirmed the result obtained by polysom-
nography. However, in adults with persistent primary
insomnia without objective changes in polysomnography,
a lower amount of delta power and elevated theta and
beta power in non-REM sleep is reported [11], proposed
to indicate hyperarousal and heightened awareness dur-
ing non-REM sleep. A similar trend was also found in the
present study concerning delta and theta power, while
beta power was on an equal level with controls. It is worth
noting that variability in beta power was considerably
larger than in the low frequencies, which might have dis-
guised the possible differences in a relatively small sam-
ple. Subjects in the study of Krystal et al. [11] also had
more severe insomnia; for example, the mean WASO in
the sleep diary was 660 min, while the corresponding fig-
ure in AS subjects was 28 min [9]. However, the power
spectral data do not indicate towards increased homeo-
static sleep pressure, which is of interest in regard to the
frequent daytime sleepiness reported by AS adults in the
sleep questionnaire [8].
Taken together, it seems that the polysomnographic
findings of the present study further confirm the hypothe-
sis emerged with the sleep questionnaire and sleep diary
studies of AS adults [8, 9] that pervasive anxiety due to AS
itself, not reflected in polysomnography, causes the sub-
jective low sleep quality in these individuals.
The degree of depressive symptoms was low, thus mak-
ing it unlikely to be reflected in polysomnographic mea-
sures. REM latency was also the same both in the AS
group and in controls.
Elia et al. [6] compared 17 autistic subjects (mean age
10 years) to 5 controls with polysomnography and found
Sleep in Young Adults with Asperger
Syndrome
shorter TIB, SP and TST as the only distinguishing fea-
tures between patients and controls. Godbout et al. [7]
published the first polysomnographic study of AS sub-
jects. They compared 8 AS subjects (age range 7–53 years)
with 8 age- and gender-matched controls and found no
difference in SE%, TST and the percent amount of sleep
stages between the groups. The results of the present study
are essentially similar, although, contrary to Godbout et
al. [7], REM sleep disruption, decreased SE% in the ear-
lier part of sleep and lower amount of sleep spindles were
not found. One confounding factor in the comparison of
different studies is that previously published studies in
this field rely mostly on categorical classifications like
DSM-IV and ICD-10, while there is no validated instru-
ment for assessing the dimensional aspect, or severity, of
autistic symptoms in adults with AS.
In order to promote compliance in AS subjects with
strict daily routines, we were not very rigorous with caf-
feine and nicotine abstinence. Anyhow, the use of these
substances was quite infrequent and should have in-
creased wakefulness and enhanced difficulties in sleep ini-
tiation [27, 28], an effect not seen in polysomnography.
AS subjects of the present study were patients from a
clinic that is specialized for the assessment of AS. Subjects
using sedatives or other psychoactive medicines were
excluded from the study, presumably excluding those sub-
jects that had severe sleep problems. Even in this popula-
tion with relatively mild AS symptoms, nearly all had
some complaint of insomnia. Although the generalizabili-
ty of our results to all adults with AS remains open, it is
obvious that a substantial proportion of AS adults display
a similar type of subjective sleep difficulties as previously
described in children with ASD. It appears that as the core
features of AS may somewhat alleviate in progression
from childhood to adulthood [1, 19], the impact of psy-
chiatric comorbidity, together with the demands of daily
social activity in adult life may play a greater role in sleep
difficulties of AS adults. This has to be verified, however,
with larger patient samples of varying degrees of impair-
ment.
Acknowledgements
We wish to thank Miss Anna-Maarit Penttilä for excellent techni-
cal assistance and Prof. Dag Stenberg for useful advice in the course
of the work. We also want to express our gratitude to Miss Susan Pihl
from The Finnish Institute of Occupational Health, for scoring the
polysomnograms. The research was funded by the Helsinki Universi-
ty Hospital (EVO: TYH 9233). Additional funding was provided by
Yrjö Jahnsson’s Foundation and The Finnish Psychiatric associa-
tion.
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