PREVALENCE AND RISK FACTOR OF EDS IN YOUNG CHILDREN

Prevalence and Risk Factors of Excessive Daytime Sleepiness in a Community

Sample of Young Children: The Role of Obesity, Asthma, Anxiety/Depression,
and Sleep
Susan L. Calhoun, PhD; Alexandros N. Vgontzas, MD; Julio Fernandez-Mendoza, PhD; Susan D. Mayes, PhD; Marina Tsaoussoglou, BS; Maria Basta, MD;
Edward O. Bixler, PhD
Sleep Research and Treatment Center, Pennsylvania State University College of Medicine, Hershey, PA

Study Objectives: We investigated the prevalence and association of excessive daytime sleepiness (EDS) with a wide range of factors (e.g.,
medical complaints, obesity, objective sleep [including sleep disordered breathing], and parent-reported anxiety/depression and sleep difficulties)
in a large general population sample of children. Few studies have researched the prevalence and predictors of EDS in young children, none in a
general population sample of children, and the results are inconsistent.
Design: Cross-sectional
Setting: Population -based.
Participants: 508 school-aged children from the general population.
Interventions: N/A
Measurements and Results: Children underwent a 9-hour polysomnogram (PSG), physical exam, and parent completed health, sleep and psy-
chological questionnaires. Children were divided into 2 groups: those with and without parent reported EDS. The prevalence of subjective EDS was
approximately 15%. Significant univariate relationships were found between children with EDS and BMI percentile, waist circumference, heartburn,
asthma, and parent reported anxiety/depression, and sleep difficulties. The strongest predictors of EDS were waist circumference, asthma, and
parent-reported symptoms of anxiety/depression and trouble falling asleep. All PSG sleep variables including apnea/hypopnea index, caffeine
consumption, and allergies were not significantly related to EDS.
Conclusions: It appears that the presence of EDS is more strongly associated with obesity, asthma, parent reported anxiety/depression, and
trouble falling asleep than with sleep disordered breathing (SDB) or objective sleep disruption per se. Our findings suggest that children with EDS
should be thoroughly assessed for anxiety/depression, nocturnal sleep difficulties, asthma, obesity, and other metabolic factors, whereas objective
sleep findings may not be as clinically useful.
Keywords: Children, excessive daytime sleepiness, obesity, anxiety/depression
Citation: Calhoun SL; Vgontzas AN; Fernandez-Mendoza J; Mayes SD; Tsaoussoglou M; Basta M; Bixler EO. Prevalence and risk factors of
excessive daytime sleepiness in a community sample of young children: the role of obesity, asthma, anxiety/depression, and sleep. SLEEP
2011;34(4):503-507.

INTRODUCTION with EDS in obese children.4,5 One population-based study on

Although excessive daytime sleepiness (EDS) in adults has
been the focus of extensive research, studies on the risk factors
associated with EDS in children have been limited. The preva-
lence of EDS in young children with sleep disordered breathing
(SDB) varies greatly, from just 7% to as high as 49%.1,2 This
variation may be explained by the different methods used for de-
termining EDS, sample size, and referral source, as well as con-
founding factors that have not been examined, such as obesity.
Although EDS in children is commonly assumed by phy-
sicians and lay persons alike to be the result of disturbed or
inadequate sleep, which in turn may interfere with daytime func-
tioning (e.g., academic performance, behavioral and psycho-
logical problems), it remains unclear whether EDS is a frequent
manifestation of SDB or disturbed sleep in young children. One
study reported a weak association with EDS and SDB in chil-
dren,3 while 2 other studies found a strong association of SDB
subjective report of sleep disturbance and behavioral problems
in children found no association between EDS and emotional
or disruptive behaviors in school.6 In children scheduled for
adenotonsillectomy, Chervin et al. reported more objectively
assessed (multiple sleep latency test) and subjectively reported
sleepiness in children with moderate SDB than controls.7,8
There have been no published general population studies of
EDS in children, as defined by parent and/or teacher report of
sleepiness during the day, with objective sleep data. Therefore,
our study is the first to report on the association between EDS
and objective measures of sleep, demographic factors, health,
and parent-reported sleep difficulties and emotional problems
in a general population of young children. The purposes of this
study were to (1) establish the prevalence of EDS, and (2) iden-
tify associations between demographic, emotional, and medical
factors and the quantity and quality of sleep—measured objec-
tively and by parent report—in young children with EDS.

Submitted for publication July, 2010 METHODS

Submitted in final revised form September, 2010
Accepted for publication September, 2010
Address correspondence to: Susan L. Calhoun, PhD, Department of Psy-
chiatry H073, Milton S. Hershey Medical Center, P.O. Box 850, Hershey,
PA 17033, Tel: (717) 531-3806; Fax: (717) 531-6491; E-mail: scalhoun@
psu.edu
SLEEP, Vol. 34, No. 4, 2011
This study was designed in 2 phases. In Phase I, general in-
formation from parents about their child’s sleep and behavioral
patterns was collected. A screening questionnaire based on the
survey published by Ali et al.,9 validated to identify children
at high risk for SDB, was sent home to parents of every stu-
dent (K-5th grade) in 4 local school districts (n = 7,312), with
503 Risk Factors for EDS in Children–Calhoun et al

Table 1—Sample characteristics
No EDS EDS
n = 431 n = 77 P was defined as a reduction of airflow of approximately 50%
Gender (% male) 51 53 0.80
Age (y) 8.5 8.7 0.36
Race (%minority) 24 25 0.05
Professional status (%) 45 41 0.53
Waist (cm) 64.7 69.2 0.001
BMI %ile 62 70 0.02
AHI 0.76 0.87 0.54
Full Scale IQ 108 105 0.11
a 78.5% response rate. The procedure for Phase II of this study
was initiated each year for 5 years by randomly selecting 200
children based on stratification for grade, gender, and risk for
SDB from the current year’s returned questionnaires. We stud-
ied 704 children in this phase. Four children did not complete
the polysomnographic (PSG) recordings; thus 700 children out
of 1000 children were included in Phase II, for a response rate
of 70%. All children from Phase II who completed the Pediatric
Sleep Questionnaire (PSQ) were included in this study. Chil-
dren diagnosed with medical problems (37.8% allergies, 13.3%
asthma, 1.2% juvenile diabetes), mental health disorders (11.1
% ADHD, 1.7% depression/anxiety, 0.8% autism), or a learning
disability (9.1%) were not excluded from the study, so that the
sample is representative of the general population. Thus, our
final sample for this study consisted of 508 children from the
Penn State Child Cohort. We contrasted the subjects who com-
pleted the PSQ and PSG with those who did not complete Phase
II. There were no significant differences between the 2 groups
on grade, sex, and risk for SDB. This study was approved by the
Institutional Review Board of Penn State College of Medicine.
Informed consent was obtained from parents of all participants,
and assent was obtained from all children prior to participation.
Sleep Laboratory
During their visit in the laboratory, all subjects underwent
a series of subjective and objective measurements. Height and
weight were recorded for each child, and body mass index
(BMI) was calculated. Waist circumference was measured.
All subjects were then evaluated for one night in sound-at-
tenuated and temperature controlled rooms. During this time,
the child’s sleep was continuously monitored for 9 hours (24
analog channel and 10 dc channel TS amplifier using Gamma
software, Grass-Telefactor Inc). A 4-channel electroencepha-
logram (EEG), 2-channel electrooculogram (EOG), and sin-
gle-channel chin and anterior bilateral tibial electromyogram
(EMG) were recorded. Throughout the night, respiration was
monitored by thermocouples at the nose and mouth (model
TCT1R, Grass Instrument Co., Quincey, MA), nasal pressure
(Validyne Engineering Corp) and thoracic and abdominal strain
gauges (model 1312 Sleepmate Technologies, Midlothian, VA).
All-night recordings of hemoglobin oxygen saturation (SpO2)
were obtained using a cardiorespiratory oximeter (model 8800,
Nonin Medical, Inc., Plymouth, MN) attached to the finger.
Snoring sounds were monitored by a sensor attached to the
throat (Sleepmate model, 1250). Our records were screened for
SLEEP, Vol. 34, No. 4, 2011
sleep apnea using criteria that are currently used clinically.10,11
An obstructive apnea was defined as a cessation of airflow of ≥
5 sec and an out-of-phase strain gauge movement. A hypopnea
with an associated decrease in oxygen saturation (SpO2) ≥ 3%
or an associated arousal. Based on these data an apnea/hypop-
nea index (A/HI) was calculated [(apnea+hypopnea)/hours of
sleep]. A long awakening was defined as ≥ 10 min.
Parent Rating Scales
For the purposes of this study, the Pediatric Sleep Question-
naire developed by Chervin12 was completed by a parent in order
to assess EDS in our study population. Children were classified
as having EDS when the parent reported “yes” for “Does your
child have a problem with sleepiness during the day?” and/or
“Has a teacher or other supervisor commented that your child
appears sleepy during the day?” The same definition of EDS
was used in a recently published study by Tsaoussoglou et al.5 A
parent also completed the Child Behavior Checklist (CBCL),13
which is a widely used tool for the assessment of childhood be-
havioral abnormalities. One of the 8 syndrome scales (anxious/
depressed) was used. In addition, a parent completed the Pedi-
atric Behavior Scale, 14 which has norm-referenced T scores for
several subscales including problems with sleep. Each item is
scored on a 0 to 3 point scale, with 0 indicating no problems and
3 indicating that a behavior is very much or very often a prob-
lem. The PBS has been used in several studies by our group to
assess sleep problems in children with autism and ADHD.15-17
Statistical Analyses
The primary objective of the analysis was to evaluate the
prevalence of EDS and associations with various risk factors,
including SDB in a general population of young children. BMI
was expressed as BMI percentiles (BMI %) adjusted for age and
gender using the formula and data of the NHANES CDC growth
charts.18 AHI was analyzed as a continuous variable. Univari-
ate analyses of these data were initially conducted to compare
those with and without a complaint of EDS with respect to vari-
ous outcomes using t-test or χ2 tests. Effect size (Cohen’s d), P
values, and odds ratios (ORs) ± 95% confidence intervals (CIs)
based on the difference between the 2 groups are reported. Bi-
nary logistic regression was used for the multivariate analysis.
The statistical confidence level selected for all analyses was P
< 0.05. All analyses were performed using Predictive Analytics
Software (PASW, Inc, Chicago, IL) Version 17.0.
RESULTS
The final sample of 508 children consisted of 431 children
without EDS and 77 children with EDS. The age range was
5-12 years, with an average age of 102.0 ± 0.08 months. Ap-
proximately one-quarter of our sample was minority(African
American, Asian and Hispanic ) as defined by a parent; (51.8%
were boys, and 45% were from a professional family. The aver-
age AHI was 0.8 ± 0.06, with only 6 children with an AHI ≥ 5.
The prevalence of EDS was 15.0% (Table 1).
The distribution of demographic factors and potential risk
factors for EDS is described in Table 2. Waist circumference,
positive history of asthma, use of asthma medication, heart-
burn, and parent reported symptoms of anxiety/depression were
504 Risk Factors for EDS in Children–Calhoun et al
significantly associated with EDS. In addition,
Table 2—Univariate associations between children with and without EDS
parent-reported symptoms of sleep difficul-
ties (i.e., trouble falling asleep, restless sleep, Risk Factors Univariate ES P ORs CI
and wakes often during the night) were also Health Heartburn 0.35 0.008 3.1 1.4, 7.2
significantly associated with EDS. The parent- Asthma 0.35 0.006 2.4 1.3, 4.3
reported sleep difficulties remained significant Asthma medication 0.41 0.002 2.9 1.5, 5.7
even when controlling for waist circumfer- Allergies 0.23 0.07 0.63 0.39, 1.03
ence, asthma, and anxiety/depression. Caffeine Caffeine consumption 0.05 0.58 1.2 0.66, 2.1
intake (weekly) and history of allergies were Waist (cm) 0.43 0.001 1.04 1.01, 1.06
not significantly associated with EDS. Objec- Objective Sleep Total sleep time 0.03 0.82 1.00 0.99, 1.01
tive sleep factors (Table 3) included AHI, min- Number of long awakenings 0.08 0.48 0.91 0.69, 1.2
imum SpO2, sleep latency, REM latency, total Sleep latency 0.03 0.82 1.00 0.99, 1.01
sleep time, number of long awakenings, sleep REM latency 0.12 0.34 1.00 0.99, 1.00
efficiency, number of arousals, and percent of %Stage 1 0.02 0.90 0.99 0.93, 1.07
REM, stage 1, 2, and slow wave sleep. None of % Stage 2 0.15 0.23 1.01 0.99, 1.04
the objective sleep factors were significantly %SW 0.15 0.23 0.99 0.96, 1.01
associated with EDS.
% REM 0.01 0.99 1.00 0.96, 1.04
In order to establish the relative indepen-
Arousal index 0.06 0.62 0.97 0.88, 1.09
dent contribution of these risk factors we
Min SpO2 0.10 0.45 0.98 0.91, 1.04
further analyzed the data from a multivariate
AHI 0.08 0.55 1.04 0.91, 1.2
perspective using binary logistic regression.
Four models were created. The most plausible Sleep efficiency 0.05 0.74 1.00 0.98, 1.04
theoretical predictors of EDS were tested be- Subjective Sleep Trouble falling asleep 0.59 < 0.001 1.7 1.4, 2.3
ginning with metabolic factors and objective Restless sleep 0.46 < 0.001 1.6 1.3, 2.0
sleep difficulties, then subjective history of Wakes often during the night 0.56 < 0.001 1.8 1.4, 2.3
medical and psychological factors, ending with Psychological Depression and/or anxiety 0.48 < 0.001 2.9 1.6, 5.1
parent-reported sleep difficulties. The initial
model included all objective sleep variables ES, Effect size Cohen’s d
and waist circumference. The second model
included all of Model 1 variables plus asthma
and heartburn. Model 3 included all variables from Model 2
plus parent-reported anxiety/depression. Model 4 included all Table 3—Objective sleep variables: Means for the children with and
variables from Model 3 plus parent-reported sleep difficulties. without EDS
Waist circumference and anxiety/depression remained indepen- No EDS EDS P value
dent predictors of EDS in Model 4, while asthma was elimi- Sleep latency (min) 28.5 ± 1.2 29.2 ± 2.7 0.67
nated from the model (Table 4). None of the objective measures Total sleep time (min) 456.9 ± 2.4 458.3 ± 4.9 0.33
of sleep, including sleep stages and AHI, were independently Sleep efficiency (%) 85.8 ± 0.41 86.1 ± 0.85 0.45
associated with EDS in any of the four models. REM latency (min) 160.1 ± 3.2 152.4 ± 6.6 0.36
Stage 1 (%) 3.6 ± 0.16 3.5 ± 0.35 0.76
DISCUSSION Stage 2 (%) 45.6 ± 0.56 47.4 ± 1.3 0.92
In our general population sample of 508 children, we ob- Slow wave (%) 31.2 ± 0.54 29.5 ± 1.3 0.79
served a prevalence of 15% for EDS. Our study indicates that REM (%) 19.7 ± 0.27 19.7 ± 5.8 0.92
EDS is highly prevalent in children, a symptom that may ad- Arousal index 3.1 ± 0.12 3.0 ± 0.26 0.42
versely affect daytime functioning. Interestingly, independent
SpO2 low* (%) 94.1 ± 0.18 93.8 ± 0.29 0.18
predictors of EDS were waist circumference, parent report of
anxiety/depressive symptoms and trouble falling asleep, as well
Mean and standard error. *Mean percentage of oxygen saturation during
as a history of asthma. respiratory events.
This study is the first to evaluate simultaneously a wide range
of potential risk factors that included demographic, medical,
psychological, objective and parent-reported sleep variables as- arousals, and percent of REM, stage 1, 2, and slow wave sleep)
sociated with EDS in a general population of young children were not significantly associated with EDS in our study. How-
(Penn State Child Cohort). This study suggests an association ever, these objective sleep findings should be considered within
between childhood EDS and medical factors (i.e., heartburn, the context of limitations that include the possible impact of
asthma), medication for asthma, waist circumference, and first-night effect and a relatively low prevalence of children with
parent-reported anxiety/depression and sleep difficulties (i.e., moderate to severe SDB in a population sample (AHI ≥ 5) af-
trouble falling asleep, restless sleep, and wakes often during fecting our power.
the night). Parent report of allergies, and objective sleep factors To assess the relative contribution of various factors for the
(AHI, minimum SpO2, sleep latency, REM latency, total sleep presence of EDS, we evaluated our data from a multivariate per-
time, number of long awakenings, sleep efficiency, number of spective. Waist circumference was the most strongly associated
SLEEP, Vol. 34, No. 4, 2011 505 Risk Factors for EDS in Children–Calhoun et al

Table 4—Risk factors for EDS based on multiple logistic regression
Model 1 Model 2 Model 3
P OR P OR P OR
Waist circumference 0.003 1.04 0.01 1.04 0.003 1.04
Asthma 0.03 2.10 0.040 2.10
Depression/Anxiety 0.010 2.50
Trouble falling asleep
Waist circumference is a continuous variable; asthma, depression/anxiety, and trouble falling asleep
are binary variables. Model 1: Waist circumference and objective sleep variables. Model 2: Waist
circumference, objective sleep, and medical variables. Model 3: Waist circumference, objective
sleep, medical, and depression/anxiety variable. Model 4: Waist circumference, objective sleep,
medical, and subjective reported depression/anxiety and sleep related variables.
with EDS. This finding is consistent with previous studies,2,4,5
demonstrating that obesity in children is independently associ-
ated with an increased risk for EDS, even in children with SDB.
Our finding that waist circumference contributes to the indepen-
dent prediction of EDS suggests that metabolic factors may play
a contributing role in the mechanism of EDS, as others have
reported in children and adults with SDB.19-21 One study4 found
that in children matched for SDB, EDS was linked to increased
levels of inflammatory mediators (e.g., Interleukin-6, high sen-
sitivity C Reactive Protein, Tumor Necrosis Factor 1), suggest-
ing that pro-inflammatory cytokines are mediators of EDS in
children similar to adults.20 Most recently a study5 comparing
obese children with mild to moderate SDB to obese children
without SDB and lean controls, suggested that obesity and SDB
were independently associated with EDS; and that inflammatory
markers and leptin increased and adiponectin decreased in these
obese children with SDB. EDS frequency increased progres-
sively and significantly in the groups, with the lowest frequency
in the lean group and the highest in the group with an AHI ≥ 5
(11%), in contrast to the results of our study, which only had 5
children with an AHI ≥ 5 (1%). This difference in the samples’
composition may help explain why SDB was not an independent
risk factor in our study. An alternative but not mutually exclu-
sive explanation is the potential influence of obesity on lung vol-
ume, which may have an impact on daytime sleepiness.
The second and third strongest independent risk factors in
our multivariate analysis were parent-reported anxiety/depres-
sion and trouble falling asleep. The anxiety/depression finding
is consistent with a recent study by Mayes et al.22 that suggests
children with a clinical diagnosis of anxiety/depression had
more daytime sleepiness than children with ADHD, autism,
brain injury, and controls. Similarly, depression was indepen-
dently associated with EDS in two studies of adults.21,23 Our
data suggest that EDS in this population of young children may
be the result of anxiety/depression that should be appropriately
evaluated and managed. The effect of anxiety and depression
on EDS could be mediated, through the known effects of these
conditions on the quality and quantity of sleep, or/and through
the activation of physiological systems such as the stress sys-
tem, that may result fatigue. Finally, the association of parent-
reported trouble falling asleep with EDS is consistent with the
fact that in adults nighttime sleep difficulties are associated with
fatigue and sleepiness. 24,25
SLEEP, Vol. 34, No. 4, 2011 506
Parent report of wheezing/nocturnal
asthma was the fourth strongest risk factor
Model 4 for EDS. When trouble falling asleep was
P OR added to the final model, asthma was elimi-
0.004 1.03 nated. This suggests that parent-reported
0.160 1.60 trouble falling asleep mediates the asso-
0.050 1.90 ciation between asthma and EDS. Thus, in
0.030 1.40 children with asthma, trouble falling asleep
may partially explain their symptoms
of EDS. This finding is supported by a
study that reported an increase in daytime
sleepiness in children who wheeze or have
asthma, with an association between a
complaint of EDS and parent reported sleep
disturbance.26 We found no association,
however, with any objective markers of
sleep between those with and without asthma (data not shown).
Our finding is compromised by the fact that one night in the lab
may not be representative of the child’s habitual sleep patterns
or seasonal exacerbation of asthma symptoms. An alternative
explanation is that the inflammatory process associated with a
chronic respiratory disease (as already reported in children with
obesity) or the side effect of asthma medications is the link to
EDS.
Although EDS is commonly assumed to be the result of dis-
turbed or inadequate sleep (quantity), it appears that in a large
general population of children representing the typical range
of SDB (i.e., mild), objective sleep was not related to EDS. In-
stead, the presence of EDS is more strongly associated with
obesity, parent-reported depression/anxiety and trouble falling
asleep, and asthma. Thus, from a clinical standpoint, profes-
sionals who evaluate and treat children with EDS should be
cognizant of comorbid risk factors associated with daytime
sleepiness. Although PSG is extremely useful in screening chil-
dren for a number of sleep disorders (i.e., narcolepsy, seizures,
parasomnias, SDB), in children with a parent complaint of
EDS, parent information regarding sleep difficulties, particular-
ly trouble falling asleep, may be more relevant. Primary lines of
treatment might include weight loss if the child is overweight,
treatment for underlying depressive and anxious symptoms,
and implementation of nocturnal asthma prevention methods
(e.g., making your bedroom free of allergens, such as dust mites
and cigarette smoke, and using a humidifier in the house to keep
the air warm and moist) if the child is diagnosed with asthma.
Future research needs to determine if children with moderate to
severe SDB (AHI ≥5) are at greater risk for EDS than children
without SDB.
ACKNOWLEDGMENTS
This work was supported by NIH grants: RO1 HL63772,
MO1 RR010732, and C06 RR016499.
DISCLOSURE STATEMENT
This was not an industry supported study. The authors have
indicated no financial conflicts of interest.
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