Sleep disorders in children

Ann C. Halbower and Carole L. Marcus

Purpose of review Introduction

Childhood sleep disorders are one of the most prevalent
complaints in the pediatrician’s office. Infant sleep rhythm
Infant sleep disorders
complaints from new mothers reach 46%, while childhood
Infant sleep-disordered breathing
obstructive sleep apnea has a prevalence of 2% and
There are more than 80 ICD-9 classified sleep disorders,
adolescent insomnia with daily consequences surpasses that
and scores of causes for both sleepiness and insomnia.
percentage.
Figure 1 illustrates the enormous variety of intrinsic and
Recent findings
extrinsic factors that influence sleep disorder presenta-
Each sleep disorder must be considered in context of age, as
tions on the developing child. Infant sleep is influenced
age influences the presentation and impact on the developing
by gestational age, environment, and parenting skills.
child or adolescent. For example, sleep-disordered breathing
Add to that the unique anatomy of an infant [1,2] com-
resulting in adult sleepiness can contribute to death in infants.
bined with an immature nervous system [3], and infant
The symptoms of narcolepsy are often masked until after
sleep develops into a separate science in sleep medicine.
adolescence, resulting in psychologically costly misdiagnoses.
Unlike apnea at other stages of development, sleep-
Summary
disordered breathing in the infant presents a unique
There are no outcome studies that track the long-term
threat to life. Apnea of prematurity, infant apnea, and
consequences of pediatric sleep disorders or their contribution
sudden infant death syndrome (SIDS) are all examples
to adult sleep problems, but this is an area of increasing
of disordered breathing or possibly disordered arousal
research interest. This review assesses the most recent
during sleep. Extensive diagnostic evaluations of infant
literature on pediatric sleep disorders from May 1, 2002, until
apnea and 30 years of apnea monitor use did not change
April 30, 2003.
the incidence of SIDS. New guidelines on infant apnea
management and monitor use are but partially based on
Keywords evidence [4] underscoring the lack of mechanistic knowl-
obstructive sleep apnea, sudden infant death syndrome, edge regarding vulnerability in these infants.
pediatric sleep disorders

Curr Opin Pulm Med 9:471–476. © 2003 Lippincott Williams & Wilkins.
Sudden infant death syndrome
In the past decade, attention to epidemiological evi-
dence caused the first worldwide decline in the inci-
dence of SIDS [5,6]. Efforts aimed at reducing modifi-
able risk factors related to SIDS, notably the prone
sleeping position, over-bundling, and smoke exposure
Eudowood Division of Pediatric Respiratory Sciences, Johns Hopkins University, reduced the SIDS incidence by more than 60% in most
Baltimore, Maryland, USA
parts of the world. Attention to the “new epidemiology”
Correspondence to Ann C. Halbower, MD, Johns Hopkins University, Division of of SIDS cases has now demonstrated a similar risk profile
Pediatric Pulmonology, 600 N. Wolfe St., Park 316, Baltimore, MD 21287 USA
E-mail: ahalbowe@jhmi.edu for infants dying unexpectedly but of known causes such
as medical disorders [7], with chaotic home environ-
Current Opinion in Pulmonary Medicine 2003, 9:471–476
ments and parental unemployment increasing the risk.
Abbreviations
OSA obstructive sleep apnea
RCT randomized controlled trial Sudden infant death syndrome is not a disease, but a
SIDS sudden infant death syndrome symptom or outcome of an underlying problem. As SIDS
© 2003 Lippincott Williams & Wilkins victims decline, there is renewed focus on what is still
1070-5287 killing the vulnerable infant, with both environmental
and intrinsic mechanisms suggested. An apparent in-
crease in the incidence of infanticide [8] merely reflects
its growing percentage in contrast to the declining post-
neonatal deaths. While the possibility of child abuse
should no longer be ignored in infant death [9], investi-
gation of the death scene, or more importantly, the sleep
471
472 Sleep and respiratory neurobiology
Figure 1. Long-term consequences of untreated childhood sleep problems
environment, is key to understanding what makes a child
vulnerable and perhaps more importantly, what keeps a
child alive [10]. Mechanistic studies focusing on the
known risk factors have shown that infants sleeping in
the prone position re-breathe exhaled gas or have oxy-
genation problems and decreased arousal [11–13], or a
more collapsible pharynx [14], risking obstruction. Ge-
netic alterations in the brainstem [15], cell function [16],
or cytokine profile [17] may cause vulnerability in some
infants. Cigarette smoke and its apparent causal relation
to SIDS has been an area of intense study [18] with
evidence for decreased arousal in smoke-exposed infants
[19,20].
There is a recent proposal for a new pathologic definition
of SIDS [21]. The term “sudden infant death syndrome”
is an exclusionary term when a cause for death cannot be
found. According to Dr. Beckwith, this term has been
used too liberally, allowing deaths to be labeled SIDS
when in fact no autopsy or death scene investigation was
performed. Other pediatric pathologists agree that it is
time for a new definition [22,23], using lessons learned
from epidemiological evidence, and also allowing for ad-
vances in cell and molecular biology to aid in research.
One cannot ignore the racial disparity in incidence of
postneonatal deaths. Infant mortality statistics from 2000
yield a death rate for low birthweight African American
infants four times that of white infants [24]. The SIDS
rate for black and Native American infants is more than
twice that of white infants. Recent case control or ques-
tionnaire studies [25,26] have blamed an increase in
prone positioning for the racial disparity in SIDS; how-
ever, other studies have demonstrated more of an impact
There are an enormous variety of intrinsic and extrinsic
factors that influence sleep disorder presentations on the
developing child. These factors can influence the
subsequent stages of development.
from infant sleep on nonstandard sleep surfaces [27•,28]
including bedsharing, which varies by culture. Bedshar-
ing was very risky in a study of Native American infant
deaths, which included a history of parental alcohol use
[29], a risk factor noted in the CESDI/SUDI study ref-
erenced previously [7]. The recently considered mecha-
nism causing death in nonstandard bedding is deficient
arousal to hypoxia or hypercapnia associated with a cov-
ered head, as can happen with soft bedding or thick
blankets on adult beds [30]. In a prospective study of
27,000 infants in Japan, an association between obstruc-
tive sleep apnea and gliosis in the raphe nuclei of the
midbrain was found in SIDS cases, but its relation to
arousal deficiency remains to be seen [31].
Infant sleep-onset association disorder
Although not life threatening, infant sleep rhythms af-
fect infant and maternal well being. In a well-designed
randomized controlled trial (RCT), infant sleep was re-
ported as abnormal in 46% of visits to the pediatric clinic
during the second 6 months of life. Early behavioral in-
tervention decreased both sleep problems and maternal
depression [32•]. In a separate RCT, sleep problems in
infants were predicted in those infants who had a high
number (>11) of feeds per day. A simple preventative
behavioral program increased the number who slept
through the night [33].
Sleep disorders of pre-pubescent child
Sleep-disordered breathing in childhood
The association of obstructive sleep apnea (OSA) with
daytime sleepiness, obesity, hypertension, and increased
cardiovascular risk in adults is recognized as a public
health problem. The signs and symptoms of OSA in chil-

dren are often confusing and recognition is not intuitive.
There is growing concern regarding the serious impacts
of OSA on childhood cardiovascular health [34–36]. An
exciting new focus on the long-term cardiovascular con-
sequences of sleep apnea in adults has led to an emerg-
ing realization that these risk profiles may be present in
childhood. There is recent evidence that OSA in adults
is linked to the metabolic syndrome [37,38], which is a
constellation of factors including diabetes, obesity, and
hypertension, associated with increased risk for cardio-
vascular mortality. These factors were linked to OSA
even corrected for BMI. There are just a few pilot stud-
ies in childhood OSA with similar findings [39], but if the
association is noted in children, the ultimate future focus
in the prevention of adult sleep apnea and cardiovascular
risk may be the management of pediatric OSA.
There is recent evidence that children with OSA dem-
onstrate a striking increase in health care utilization be-
fore diagnosis [40•]. This study showed a greater than
220% increase in hospitalizations, drug use, and emer-
gency visits in patients with OSA, not accounting for
other life impact measures such as missed school or pa-
rental absence. Obstructive sleep apnea in children is
common, with a prevalence of 2% [41] and a peak age
range of 2 to 6 years, which historically was assumed to
be related to the relative adenotonsillar hypertrophy at
this age range. Arens et al. [42] have demonstrated what
others assumed using imaging studies to confirm that the
overlap of adenoids and tonsils contribute to airway nar-
rowing along a long segment of the upper airway in chil-
dren with OSA.
Although there are many reports on the association of
cognitive impacts of sleep apnea in adults [43], the
mechanism for that association is not known. Parental
reports of conduct problems, hyperactive behavior, and
inattention [44,45], as well as quality of life [46,47] are
linked to sleep-disordered breathing. Important studies
have demonstrated worrisome learning impairments in
rodents exposed to intermittent hypoxia, where juvenile
animals corresponding to the age of adenotonsillar hy-
pertrophy in children were affected [48]. Although learn-
ing impairment and school performance abnormalities
have been suggested in children with OSA [49–51], re-
search is still required regarding the most vulnerable age
groups or the potential reversibility of consequences.
Of note in the literature of the past year is the American
Academy of Pediatrics Clinical Practice Guideline re-
garding the diagnosis and management of childhood
OSA syndrome [52•]. This guideline gives the practitio-
ner an algorithm for screening, diagnosing, and treating
OSA in the general pediatric population.
Diagnosing sleep-disordered breathing
The gold standard of diagnosis of sleep apnea is the
polysomnogram. Recently, the use of nasal pressure
transducers has improved the diagnostic sensitivity of
Sleep disorders in children Halbower and Marcus 473
the polysomnogram in terms of airflow limitation [53,54]
and can be used in children as young as 2 years old for at
least half of the night. The notable problem with the
cannula in these studies is the significant amount of time
without signal in children since they are pulled off or
dislodged. A simultaneous back-up system such as the
thermistor might be considered. Pulse transit time now
aids in the recognition of arousals, which normally de-
pend on the accuracy of EEG scoring [55•,56]. In chil-
dren, movement artifact has impaired the diagnostic use-
fulness of pulse-oximetry during sleep. New technology
that decreases these false–negative events is now avail-
able. The Masimo oximeter was compared with the
Nellcor 200 and found to be superior in event detection
during movement [57]. When the averaging time was
reduced to 2 seconds, more short saturation declines
were detected.
Managing sleep-disordered breathing
There is a serious paucity of pediatric randomized con-
trolled trials regarding OSA treatment efficacy as pointed
out in the past year’s Cochrane database [58]. Clinical
evaluations of treatment effect usually focus on before-
and-after improvements in behavior or respiratory distur-
bance index.
Adenotonsillectomy has been shown to resolve respira-
tory disturbance [59] and symptoms [60] in 75 to 100% of
otherwise healthy children, and is considered first-line
therapy in children with otherwise normal craniofacial
features. Continuous positive airway pressure applied
nasally has become a good second-line therapy of OSA in
children when adenotonsillectomy fails or is contraindi-
cated. A study shows that a period of home acclimatiza-
tion with the mask may improve acceptance [61] and
other desensitization methods have been found useful in
young children [62,63].
Common parasomnias
Sleep walking, talking, and night terrors are so common
in children that they are often considered normal by pe-
diatricians. As disorders of arousal, they can be induced
by severe fatigue or illness. A retrospective study on a
group of children referred to sleep clinic (with its obvious
referral bias) suggested that many children with chronic
sleep terrors should be investigated for sleep-disordered
breathing. They saw an association between chronic
sleep terrors and sleep disordered breathing in 61% of
cases [64]. The parasomnias disappeared after surgical
management of obstructive apnea.
A brief mention of other childhood sleep disorders in the
literature of the past year should include a nice review on
childhood rhythmic movement disorders with treatment
suggestions provided by Timothy Hoban [65]. An inter-
esting complex segregation analysis suggested an auto-
somal dominant gene involved in patients with restless
474 Sleep and respiratory neurobiology
legs syndrome in people presenting with symptoms be-
fore the age of 30 [66]. Nightmares, common before the
age of 10 years, were found to be associated with trait
anxiety in school-aged children [67], indicating the need
to observe these children. Seizure disorders often pre-
sent in childhood or adolescence and are frequent find-
ings in the pediatric sleep lab due to the close association
of certain sleep states with epilepsy. An updated review
of this childhood phenomenon was provided by D. Din-
ner of the Cleveland Clinic Foundation [68].
Sleep disorders of adolescents
It is no wonder that adolescent medicine has branched
off as a separate area of pediatrics. Not only is the obvi-
ous change in puberty a factor in disease and psychologi-
cal health, but several sleep disorders, circadian prefer-
ence, and changes in lifestyle all impact adolescent
sleep, or the lack of it. There can be long-term conse-
quences of untreated childhood sleep problems that af-
fect the adolescent, as illustrated in Figure 1. A well-
done longitudinal study on 490 children demonstrated
that sleep problems at age 4 years predicted behavioral/emo-
tional problems in mid-adolescence. The correlation of
sleep problems with depression, anxiety, and attention
problems increased with time [69].
Insomnia
Insomnia has been considered the most common sleep
disorder in adolescents, with a prevalence ranging be-
tween 2.2 and 17% depending on whether the dysfunc-
tion is non-restorative sleep, sleep disruption, difficulty
initiating sleep, or disturbed sleep impacting on daytime
functioning [70]. Indeed, pediatricians were found to be
more likely to prescribe clonidine for sleep problems
than child psychiatrists (67 vs. 50%) [71]. In a prospec-
tive study of more than 4000 adolescents, insomnia was
linked to impaired daytime function [70]. Insomnia was
linked to current or past mental disorders in another
study [72]. The obvious question, “Does insomnia cause
mental disturbance and dysfunction, or the reverse?”,
has not been determined. Unfortunately, the reviews
[73] and longitudinal studies of the past year only un-
derscore the questions. Whether early treatment of pe-
diatric insomnia can disrupt its negative impact on ado-
lescent mental health remains to be studied.
Excessive sleepiness: circadian rhythm disorder
A fascinating update on the regulation of sleepiness in
adolescents was recently published by Mary Carskadon,
who spearheaded a longitudinal study on adolescent
sleep patterns as they change through puberty [74]. She
shows MSLT and biochemical data across adolescence
on circadian rhythm delays that cause conflict with
forced wake-up times. The school wake-up time is close
to the sleepiest circadian time point, and thus, a sleepy
adolescent goes to school. In a separate review, sleepi-
ness was linked to learning, memory, and attention prob-
lems, but the review did not always separate sleepiness
caused by sleep-disordered breathing, which may cause
learning problems via other mechanisms [75].
Excessive sleepiness: narcolepsy
Narcolepsy in children may present merely with exces-
sive daytime sleepiness, without demonstrating cata-
plexy or other symptoms until after adolescence [76].
Children can be misdiagnosed with psychiatric disorders
or labeled as lazy. Cerebrospinal fluid for hypocretin lev-
els in addition to HLA typing and the MSLT now aids in
the diagnosis [77,78].
Excessive sleepiness: Kleine-Levin syndrome
The rare Kleine-Levin syndrome typically presents in
adolescents and a recent systematic investigation sheds
new light on what should be considered “typical” in the
presentation. There is a predominance of males, 25
males to 5 females, with a mean age of onset of 15 years.
The episodes of severe hypersomnia and mood distur-
bance were present in all patients but variability was
observed in the exact mood change, between aggressive-
ness to reduced psychomotor activity. Hyperphagia was
present in 57% and sexual disinhibition in 47%, so that
they were not necessary to meet the criteria for diagnosis.
For the first time, an association with HLA-DQB1*0201
was noted by the authors [79].
References and recommended reading
Papers of particular interest, published within the annual period of review,
have been highlighted as:
• Of special interest
•• Of outstanding interest
1 Hershenson MB: The Respiratory Muscles and Chest Wall. In Respiratory
Control Disorders in Infants and Children. Edited by Beckerman RC, Brouil-
lette RT, Hunt CE. Baltimore: Williams & Wilkins; 1992:28–46.
2 Henderson-Smart DJ, Read DJ: Reduced lung volume during behavioral ac-
tive sleep in the newborn. J Appl Physiol 1979, 46:1081–1085.
3 Halbower AC, Jones MD Jr: Physiologic reflexes and their impact on resus-
citation of the newborn. Clin Perinatol 1999, 26:621–627.
4 Committee on Fetus and Newborn. American Academy of Pediatrics. Apnea:
sudden infant death syndrome, and home monitoring. Pediatrics 2003,
111:914–917.
5 Leach CE, Blair PS, Fleming PJ, et al.: Epidemiology of SIDS and explained
sudden infant deaths. CESDI SUDI Research Group. Pediatrics 1999,
104:e43.
6 Stewart A, Mitchell EA, Tipene-Leach D, et al.: Lessons from the New Zealand
and UK cot death campaigns. Acta Paediatr Suppl 1993, 82(suppl
389):119–123.
7 Platt MW, Blair PS, Fleming PJ, et al.: A clinical comparison of SIDS and
explained sudden infant deaths: how healthy and how normal? CESDI SUDI
Research Group. Confidential Inquiry into Stillbirths and Deaths in Infancy
study. Arch Dis Child 2000, 82:98–106.
8 Krous HF, Nadeau JM, Silva PD, et al.: Infanticide: is its incidence among
postneonatal infant deaths increasing?: an 18-year population-based analy-
sis in California. Am J Forensic Med Pathol 2002, 23:127–131.
9 Truman TL, Ayoub CC: Considering suffocatory abuse and Munchausen by
proxy in the evaluation of children experiencing apparent life-threatening
events and sudden infant death syndrome. Child Maltreat 2002, 7:138–148.
10 Blair P, Fleming P: Epidemiological investigation of sudden infant death syn-
drome infants—recommendations for future studies. Child Care Health Dev
2002, 28(suppl 1):49–54.
11 Patel AL, Paluszynska D, Harris KA, et al.: Occurrence and mechanisms of

sudden oxygen desaturation in infants who sleep face down. Pediatrics 2003,
111:e328–e332.
12 Horne RS, Bandopadhayay P, Vitkovic J, et al.: Effects of age and sleeping
position on arousal from sleep in preterm infants. Sleep 2002, 25:746–750.
13 Horne RS, Ferens D, Watts AM, et al.: The prone sleeping position impairs
arousability in term infants. J Pediatr 2001, 138:811–816.
14 Ishikawa T, Isono S, Aiba J, et al.: Prone position increases collapsibility of the
passive pharynx in infants and small children. Am J Respir Crit Care Med
2002, 166:760–764.
15 Kinney HC, Filiano JJ, White WF: Medullary serotonergic network deficiency
in the sudden infant death syndrome: review of a 15-year study of a single
dataset. J Neuropathol Exp Neurol 2001, 60:228–247.
16 Ackerman MJ, Siu BL, Sturner WQ, et al.: Postmortem molecular analysis of
SCN5A defects in sudden infant death syndrome. JAMA 2001, 286:2264–
2269.
17 Gordon AE, MacKenzie DA, El Ahmer OR, et al.: Evidence for a genetic com-
ponent in sudden infant death syndrome. Child Care Health Dev 2002,
28(suppl 1):27–29.
18 Nattie E, Kinney H: Nicotine, serotonin, and sudden infant death syndrome.
Am J Respir Crit Care Med 2002, 166:1530–1531.
19 Chang AB, Wilson SJ, Masters IB, et al.: Altered arousal response in infants
exposed to cigarette smoke. Arch Dis Child 2003, 88:30–33.
20 Horne RS, Ferens D, Watts AM, et al.: Effects of maternal tobacco smoking,
sleeping position, and sleep state on arousal in healthy term infants. Arch Dis
Child Fetal Neonatal Ed 2002, 87:F100–F105.
21 Beckwith JB: Defining the sudden infant death syndrome. Arch Pediatr Ado-
lesc Med 2003, 157:286–290.
22 Cutz E: New Challenges for SIDS Research. Arch Pediatr Adolesc Med
2003, 157:292–293.
23 Berry PJ: SIDS: permissive or privileged ⬘diagnosis⬘? Arch Pediatr Adolesc
Med 2003, 157:293–294.
24 Mathews TJ, Menacker F, MacDorman MF: Infant mortality statistics from the
2000 period linked birth/infant death data set. Natl Vital Stat Rep 2002,
50:1–28.
25 Hauck FR, Moore CM, Herman SM, et al.: The contribution of prone sleeping
position to the racial disparity in sudden infant death syndrome: The Chicago
Infant Mortality Study. Pediatrics 2002, 110:772–780.
26 Moon RY, Omron R: Determinants of infant sleep position in an urban popu-
lation. Clin Pediatr (Phila) 2002, 41:569–573.
27 Unger B, Kemp JS, Wilkins D, et al.: Racial disparity and modifiable risk fac-
• tors among infants dying suddenly and unexpectedly. Pediatrics 2003,
111:E127–E131.
Death scene information collected after the back-to-sleep campaign demonstrated
that African American infants were much more likely to sleep in non-standard beds
such as adult beds or sofa, but differences in prone positioning were not significant.
28 Rasinski KA, Kuby A, Bzdusek SA, et al.: Effect of a sudden infant death
syndrome risk reduction education program on risk factor compliance and
information sources in primarily black urban communities. Pediatrics 2003,
111:e347–e354.
29 Iyasu S, Randall LL, Welty TK, et al.: Risk factors for sudden infant death
syndrome among northern plains Indians. JAMA 2002, 288:2717–2723.
30 Franco P, Lipshutz W, Valente F, et al.: Decreased arousals in infants who
sleep with the face covered by bedclothes. Pediatrics 2002, 109:1112–
1117.
31 Sawaguchi T, Franco P, Kato I, et al.: Interaction between apnea, prone sleep
position and gliosis in the brainstems of victims of SIDS. Forensic Sci Int
2002, 130:S44–S52.
32 Hiscock H, Wake M: Randomised controlled trial of behavioural infant sleep
• intervention to improve infant sleep and maternal mood. BMJ 2002,
324:1062–1065.
Important results from a randomized controlled trial of 156 mothers of infants 6 to
12 months of age demonstrate that behavioral intervention performed early in the
course of sleep problem development can have impacts on child and maternal
depression.
33 Nikolopoulou M, James-Roberts I: Preventing sleeping problems in infants
who are at risk of developing them. Arch Dis Child 2003, 88:108–111.
34 Amin RS, Kimball TR, Bean JA, et al.: Left ventricular hypertrophy and abnor-
mal ventricular geometry in children and adolescents with obstructive sleep
apnea. Am J Respir Crit Care Med 2002, 165:1395–1399.
35 O’Brien LM, Gozal D: Behavioural and neurocognitive implications of snoring
Sleep disorders in children Halbower and Marcus 475
and obstructive sleep apnoea in children: facts and theory. Paediatr Respir
Rev 2002, 3:3–9.
36 Kwok KL, Ng DK, Cheung YF: BP and arterial distensibility in children with
primary snoring. Chest 2003, 123:1561–1566.
37 Punjabi NM, Sorkin JD, Katzel LI, et al.: Sleep-disordered breathing and insu-
lin resistance in middle-aged and overweight men. Am J Respir Crit Care Med
2002, 165:677–682.
38 Vgontzas AN, Chrousos GP: Sleep, the hypothalamic-pituitary-adrenal axis,
and cytokines: multiple interactions and disturbances in sleep disorders. En-
docrinol Metab Clin North Am 2002, 31:15–36.
39 de la Eva RC, Baur LA, Donaghue KC, et al.: Metabolic correlates with ob-
structive sleep apnea in obese subjects. J Pediatr 2002, 140:654–659.
40 Reuveni H, Simon T, Tal A, et al.: Health care services utilization in children
• with obstructive sleep apnea syndrome. Pediatrics 2002, 110:68–72.
A novel approach to view the impact of sleep apnea in children. The increased use
of health services was prior to diagnostic testing or treatment for OSA.
41 Redline S, Tishler PV, Schluchter M, et al.: Risk factors for sleep-disordered
breathing in children. Associations with obesity, race, and respiratory prob-
lems. Am J Respir Crit Care Med 1999, 159:1527–1532.
42 Arens R, McDonough JM, Corbin AM, et al.: Upper airway size analysis by
magnetic resonance imaging of children with obstructive sleep apnea syn-
drome. Am J Respir Crit Care Med 2003, 167:65–70.
43 Montplaisir J, Bedard MA, Richer F, et al.: Neurobehavioral manifestations in
obstructive sleep apnea syndrome before and after treatment with continuous
positive airway pressure. Sleep 1992, 15:S17–S19.
44 Chervin RD, Archbold KH, Dillon JE, et al.: Inattention, hyperactivity, and
symptoms of sleep-disordered breathing. Pediatrics 2002, 109:449–456.
45 Goldstein NA, Fatima M, Campbell TF, et al.: Child behavior and quality of life
before and after tonsillectomy and adenoidectomy. Arch Otolaryngol Head
Neck Surg 2002, 128:770–775.
46 De Serres LM, Derkay C, Sie K, et al.: Impact of adenotonsillectomy on quality
of life in children with obstructive sleep disorders. Arch Otolaryngol Head
Neck Surg 2002, 128:489–496.
47 Rosen CL, Palermo TM, Larkin EK, et al.: Health-related quality of life and
sleep-disordered breathing in children. Sleep 2002, 25:657–666.
48 Row BW, Kheirandish L, Neville JJ, et al.: Impaired spatial learning and hyper-
activity in developing rats exposed to intermittent hypoxia. Pediatr Res 2002,
52:449–453.
49 Gozal D: Sleep-disordered breathing and school performance in children.
Pediatrics 1998, 102:616–620.
50 Gozal D, Pope DW Jr: Snoring during early childhood and academic perfor-
mance at ages thirteen to fourteen years. Pediatrics 2001, 107:1394–1399.
51 Blunden S, Lushington K, Kennedy D, et al.: Behavior and neurocognitive
performance in children aged 5-10 years who snore compared to controls. J
Clin Exp Neuropsychol 2000, 22:554–568.
52 Clinical practice guideline: diagnosis and management of childhood obstruc-
• tive sleep apnea syndrome. Pediatrics 2002, 109:704–712.
Timely guidelines based on the best literature available regarding diagnosis and
treatment of obstructive sleep apnea.
53 Serebrisky D, Cordero R, Mandeli J, et al.: Assessment of inspiratory flow
limitation in children with sleep-disordered breathing by a nasal cannula pres-
sure transducer system. Pediatr Pulmonol 2002, 33:380–387.
54 Trang H, Leske V, Gaultier C: Use of nasal cannula for detecting sleep apneas
and hypopneas in infants and children. Am J Respir Crit Care Med 2002,
166:464–468.
55 Poyares D, Guilleminault C, Rosa A, et al.: Arousal, EEG spectral power and
• pulse transit time in UARS and mild OSAS subjects. Clin Neurophysiol 2002,
113:1598–1606.
Very well done study demonstrating the importance of PTT as a new technology to
improve accuracy on arousal scoring, with some specificity limitations described.
56 Katz ES, Lutz J, Black C, et al.: Pulse transit time as a measure of arousal and
respiratory effort in children with sleep-disordered breathing. Pediatr Res
2003, 53:580–588.
57 Brouillette RT, Lavergne J, Leimanis A, et al.: Differences in pulse oximetry
technology can affect detection of sleep-disorderd breathing in children.
Anesth Analg 2002, 94:S47–S53.
58 Lim J, McKean M: Adenotonsillectomy for obstructive sleep apnoea in chil-
dren. Cochrane Database Syst Rev 2003, CD003136.
59 Darrow DH, Siemens C: Indications for tonsillectomy and adenoidectomy.
Laryngoscope 2002, 112:6–10.
476 Sleep and respiratory neurobiology
60 Suen JS, Arnold JE, Brooks LJ, et al.: Adenotonsillectomy for treatment of
obstructive sleep apnea in children. Arch Otolaryngol Head Neck Surg 1995,
121:525–530.
61 Massa F, Gonsalez S, Laverty A, et al.: The use of nasal continuous positive
airway pressure to treat obstructive sleep apnoea. Arch Dis Child 2002,
87:438–443.
62 Lucas P, Liabo K, Roberts H, et al.: Do behavioural treatments for sleep dis-
orders in children with Down’s syndrome work? Arch Dis Child 2002,
87:413–414.
63 Rains JC: Treatment of obstructive sleep apnea in pediatric patients. Behav-
ioral intervention for compliance with nasal continuous positive airway pres-
sure. Clin Pediatr (Phila) 1995, 34:535–541.
64 Guilleminault C, Palombini L, Pelayo R, et al.: Sleepwalking and sleep terrors
in prepubertal children: what triggers them? Pediatrics 2003, 111:e17–e25.
65 Hoban TF: Rhythmic movement disorder in children. CNS.Spectr 2003,
8:135–138.
66 Winkelmann J, Muller-Myhsok B, Wittchen HU, et al.: Complex segregation
analysis of restless legs syndrome provides evidence for an autosomal dom-
inant mode of inheritance in early age at onset families. Ann Neurol 2002,
52:297–302.
67 Mindell JA, Barrett KM: Nightmares and anxiety in elementary-aged children:
is there a relationship. Child Care Health Dev 2002, 28:317–322.
68 Dinner DS: Effect of sleep on epilepsy. J Clin Neurophysiol 2002, 19:504–
513.
69 Gregory AM, O’Connor TG: Sleep problems in childhood: a longitudinal
study of developmental change and association with behavioral problems. J
Am Acad Child Adolesc Psychiatry 2002, 41:964–971.
70 Roberts RE, Roberts CR, Chen IG: Impact of insomnia on future functioning
of adolescents. J Psychosom Res 2002, 53:561–569.
71 Efron D, Hiscock H, Sewell JR, et al.: Prescribing of psychotropic medications
for children by Australian pediatricians and child psychiatrists. Pediatrics
2003, 111:372–375.
72 Ohayon MM, Roth T: Place of chronic insomnia in the course of depressive
and anxiety disorders. J Psychiatr Res 2003, 37:9–15.
73 Dahl RE, Lewin DS: Pathways to adolescent health sleep regulation and be-
havior. J Adolesc Health 2002, 31:175–184.
74 Carskadon MA, Acebo C: Regulation of sleepiness in adolescents: update,
insights, and speculation. Sleep 2002, 25:606–614.
75 Fallone G, Owens JA, Deane J: Sleepiness in children and adolescents: clini-
cal implications. Sleep Med Rev 2002, 6:287–306.
76 Wise MS, Lynch J: Narcolepsy in children. Semin Pediatr Neurol 2001,
8:198–206.
77 Tsukamoto H, Ishikawa T, Fujii Y, et al.: Undetectable levels of CSF hypocre-
tin-1 (orexin-A) in two prepubertal boys with narcolepsy. Neuropediatrics
2002, 33:51–52.
78 Guilleminault C, Pelayo R: Narcolepsy in children: a practical guide to its
diagnosis, treatment and follow-up. Paediatr Drugs 2000, 2:1–9.
79 Dauvilliers Y, Mayer G, Lecendreux M, et al.: Kleine-Levin syndrome: an au-
toimmune hypothesis based on clinical and genetic analyses. Neurology
2002, 59:1739–1745.