lable at ScienceDirect

Sleep Medicine Reviews 13 (2009) 355–361

Contents lists avai

Sleep Medicine Reviews

journal homepage: www.elsevier .com/locate/smrv

CLINICAL REVIEW

Risk factors and consequences of early childhood dyssomnias:New perspectives

Evelyne Touchette a,b, Dominique Petit a, Richard E. Tremblay b,c,d,e, f,g, Jacques Y. Montplaisir a,f,*

a Sleep Research Centre, Sacre-Coeur Hospital, 5400 Gouin Blvd. West, Montreal, Quebec, Canada H4 J 1C5b Paris Sud Innovation Group in Adolescent Mental Health, Inserm U669, Paris, Francec Research Unit on Children’s Psychosocial Maladjustment, Quebec, Canadad Department of Pediatrics, University of Montreal, Quebec, Canadae Department of Psychology, University of Montreal, Quebec, Canadaf Department of Psychiatry, University of Montreal, Quebec, Canadag School of public Health and Population Sciences, University College Dublin, Ireland

Keywords:DyssomniasSleep durationEarly childhoodRisk factorsConsequencesModel

* Corresponding author. Sleep Research Centre,Gouin Blvd. West, Montreal, Quebec, Canada H4J 1fax: þ1 514 338 2531.

E-mail address: jy.montplaisir@umontreal.ca (J.Y. M

1087-0792/$ – see front matter � 2008 Elsevier Ltd.doi:10.1016/j.smrv.2008.12.001

s u m m a r y

Dyssomnias are largely under-diagnosed in infants and toddlers. This literature review proposes anintegrative model based on empirical data on determinants and consequences of sleep disturbancesoccurring in early life. This model proposes that parental behaviors that impede the child’s autonomytoward sleep periods are primary grounds for the development of dyssomnias, e.g., parental presenceuntil the child falls asleep, and putting an already sleeping child to bed. The model also indicates theserious potential consequences of a modest but chronic loss of sleep in childhood. At least threedevelopmental domains could be directly affected: behavioral/social competence, cognitive performance,and physical condition. Thus, children with short nocturnal sleep duration before age 3.5 years showincreased risk of high hyperactivity–impulsivity scores and low cognitive performance at 6 yearscompared to children who sleep 11 h per night, after controlling for potentially confounding variables.Moreover, persistent short sleep duration in early infancy increased the risk of suffering of obesity at 6years of age, after controlling for potentially confounding variables. Finally, the importance of allowingthe child to sleep at least 10 h per night in early childhood is stressed, as the National Sleep FoundationPoll suggests, for optimal child development.

� 2008 Elsevier Ltd. All rights reserved.

Introduction

Although sleep plays an important role in many areas of childdevelopment, including health, mood, cognition and academicperformance,1,2 longitudinal studies of normal sleep and sleepproblems in early childhood have been conducted only recently.This literature review summarizes the results derived from thecurrent knowledge on potential determinants and consequencesof sleep disturbances occurring in early life. A model supportedby empirical data is presented, with recommendations forclinicians and parents coping with sleep problems in youngchildren.

Sacre-Coeur Hospital, 5400C5. Tel.: þ1 514 338 2693;

ontplaisir).

All rights reserved.

Normal sleep development

Sleep duration and consolidation

Normally, full-term babies sleep around 16–18 h per day atbirth, interrupted by waking periods. Total sleep duration declinesas children grow up: 13–14 h at 6 months and 10–11 h at 6 years.3

This reduction results largely from the decreasing number andduration of naps. Conversely, waking periods gradually increaseduring the daytime. Daytime sleep becomes well-defined naps: 2–3naps per day until age 6 months (3.5 h total), followed by 2 naps perday at around 9–12 months, and finally, 1 nap in the afternoon after18 months (2.5 h) up to age 3 years.4,5 Around 68% of children havestopped taking a nap by age 4 years.5

At 6 months, the longest uninterrupted nocturnal sleep period isgenerally 6 h, increasing progressively thereafter to 8–9 consecu-tive hours by the first birthday.6 An Italian study estimated that thelongest nocturnal sleep period in infants aged 6–12 months is 8–

E. Touchette et al. / Sleep Medicine Reviews 13 (2009) 355–361356

9 h, whereas children aged 13 months to 4 years had a consolidatedsleep period longer than 9 h per night.5 Nocturnal sleep durationremains almost the same (around 10–11 h) throughout the entirepreschool period.3,7,8

Sleep-wake development

Sleep-wake periods are regulated by 2 processes: 1) ‘‘Process C’’or the circadian process controls wake propensity as a sinus func-tion over a 24-hour period, and 2) ‘‘Process S’’ or the homeostaticprocess, increases exponentially during wakefulness and decreasesduring sleep (the hourglass principle).9

Process C, also termed ‘‘biological clock’’, is mainly controlled bycells located in the suprachiasmatic nuclei of the hypothalamus.10

The human SCN has been detected as early as week 18 of gesta-tion so it is formed during the first trimester of pregnancy. It wasshown through immunocytochemistry, however, that the SCNcontinues to mature after birth to reach only at one year of agethe number of vasopressin neurons observed in adults.11 Therhythmic oscillations of the clock are the result of the oscillatingexpression of transcriptional activating factors (proteins) alsoregulated by cytochromes. A number of interrelated circadiangenes ensuring that function have been identified, such as per,clock, tim, cry and Bmal12).

Because the intrinsic rhythm of the SCN is not exactly 24 h, itneeds to be reset each day to prevent the rhythm to be driftingout of sync with the light-dark cycle. One necessary pathway isthe retinohypothalamic tract which allows the light signalreceived by the retina to entrain the rhythm of the SCN. This tractis present at birth in humans but it is not certain that it is func-tionally responsive to light yet. Studies on primates suggest that itmight be.13,14

In newborns, the sleep-wake rhythm is free running. At 1month, the sleep-wake rhythm is ultradian with a period of 3–4 hthroughout the day and night.6 At 6 weeks, infants are more awakeduring the daytime than during the night and more asleep duringnighttime than during the day and at 12 weeks, periods of wake-fulness and sleep consolidate even further into a circadianpattern.13,14 External zeitgebers (e.g., light-dark cycle, noise, andsocial interactions) facilitate the establishment of the circadiansleep-wake rhythm. Different circadian rhythms (e.g., coretemperature, melatonin) develop at different rates. For example,core temperature starts to follow a circadian rhythm from the firstweek of life, whereas the circadian rhythm of melatonin secretionappears at approximately 1.5 months and that of cortisol secretionappears after 3–6 months of age.15

Process S is less well defined neurophysiologically than ProcessC. Different signals were suggested as markers of the homeostaticprocess such as stage 4 of nonrapid eye movement sleep and EEGpower density in the low-frequency range (0.75–4.5 Hz, delta orslow-wave activity).9 While the influence of Process C begins uponbirth, Process S emerges around 2 months.16

Babies’ cries decrease at the end of the day around 2 months ofage. It could be explained by the emergence of the Process S aroundthat age; the Process S might help to decrease the intensity of the‘‘wake signal’’ (Process C) at the end of the day.17

Babies need to do frequent naps. The need to do frequent napsdecreases with age. This could be explained by the fact that theaccumulation rate of sleep pressure (Process S) slows down asinfants get older, which leads to a progressive reduction in napsbecause the child can sustain wakefulness for longer periods.18

Sleep is more consolidated as the infants get older. It could beexplained by the fact that the ‘‘wake signal’’ of the Process C duringthe day gets stronger and counteracts the accumulation of sleeppressure. In the same way, the ‘‘sleep signal’’ sent by Process C

during the night hours counteracts the progressive loss of sleeppressure that could have resulted in an early awakening.18

In sum, the progress in proper alignment of Process C andProcess S in the few months after birth allows long periods ofwakefulness during the day and good sleep consolidation at night.18

In adulthood, these 2 processes contribute about equally to main-tain a consolidated bout of wakefulness throughout the day anda consolidated bout of sleep at night.19

It is well established that the timing of the sleep period starts todelay with the advent of puberty.20 It was also demonstrated thatthe displacement of the sleep period toward later hours starts earlyin life: a small phase delay was seen between 4- and 6-year-oldchildren, and later bedtimes on the weekend were associated withshorter sleep duration.21

Dyssomnias

Definitions and prevalence

Dyssomnias are defined in the DSM-IV22 as a group of disorderscharacterized by difficulty in initiating or maintaining sleep. Dys-somnias are largely under-diagnosed in infants and toddlers.22 Arecent study23 has recommended standard criteria to diagnose 2categories of sleep problems in early childhood: 1) frequentnocturnal awakenings, defined as >2 signaled awakenings/night in1–2-year-old children and>1 signaled awakening/night in children2 years old and older), and 2) sleep onset difficulties, e.g., >30 minto fall asleep in 1–2 year-old children and >20 min to fall asleep inchildren 2 years old and older. Problem severity was classified into3 categories based on frequency: a) normal (once a week or less), b)perturbation (2–4 nights per week), and c) disorder (5–7 nights perweek for more than 1 month).

These criteria are based on parental reports. Nevertheless,several objective measures obtained by actigraphy,24 video,23 andpolysomnography at home25 and in the sleep laboratory26

revealed that infants wake up on average 3 times per night frombirth to 3 years. The problem stems more from the child’sresponse (either signaling the awakening or self-soothing back tosleep) than from the awakening itself. At birth, 95% of infantssignal awakenings at night, and at age 5 months, 20% of infantssignal at least 1 awakening per night.27 However, most childrenare able to self-sooth and fall asleep on their own by the time theyare 1-year-old.28

The average sleep onset latency (time to fall asleep) remainsconstant throughout infancy at 15�10 min.25 A sleep onsetproblem is defined as a sleep latency of more than 30 min.5,23,29

Infants (younger than 2 years) suffer more from frequent nocturnalawakenings whereas sleep onset difficulties arise later in childhoodand increase across the first 4 years: from 6% at 1 year to 12% at 2years, 24% at 3 years, 49% at 4 years, and 33% at 5 years.29

Approximately 10% of young children have both sleep problemsconcurrently.6,30,31

Etiology of dyssomnias in early childhood

Nocturnal awakenings and sleep onset problems are linked toimpaired sleep consolidation, and therefore to shorter nocturnalsleep duration. Dyssomnias, or sleep fragmentation, are influencedby a combination of biological (maturation of the central nervoussystem, child’s characteristics, genetics) and environmentalfactors.32,33 A twin study in adults showed that 50% of the variancefor risk of insomnia can be attributed to genetic factors.34

Conversely, it is well-known that other biological and environ-mental factors are associated with dyssomnias in infants.

E. Touchette et al. / Sleep Medicine Reviews 13 (2009) 355–361 357

Infant characteristics

Infant characteristics are thought to influence the establish-ment of sleep consolidation. There are major discrepancies withregard to the contribution of prenatal and perinatal difficulties tosleep disturbance in children. For example, one study28 has foundassociations between poor sleep consolidation and perinataldifficulties such as lengthy delivery, low state score at birth, lowbirth weight, prematurity, and low Apgar score, whereas otherstudies found no such relationships.35–37 However, it was foundthat children who were born prematurely had a slightly higherapnea index, a slightly higher apnea–hypopnea index, slightlylower oxygen saturation at 8–11 years of age than age-matchedchildren born at term.38

For gender, there are also mixed results. One study30 showedthat boys signal awakenings more than girls, whereas anotherstudy39 observed that girls aged 4–12 months signal awakeningsmore than boys. In general, gender had no major impact on thedevelopment of sleep consolidation.23,29

A difficult temperament has been associated with sleep prob-lems.31,32,40 Preschool children with difficult temperaments,defined as irritable, fussy, easily disturbed by changes in theirenvironment, crying a lot and reacting intensely, are more likely tosignal nocturnal awakenings. A representative population-basedstudy41 revealed that a difficult temperament is a significant andindependent risk factor for poor sleep consolidation, for instance,sleeping less than 6 consecutive hours per night in early childhood.On the other hand, poor sleepers were more frequently rated ashaving a difficult temperament and more temper tantrums, andachieved higher scores on emotional and behavioral problem scalescompared to good sleepers.32 It is therefore difficult to distinguishcause from effect in this case. Children who signaled awakeningshad lower sensory thresholds compared to children who did notsignal awakenings.40

Children with organic disorders, such as gastrointestinal reflux,colic or milk allergies, show in general more sleep problems. Infantsand young children with gastrointestinal reflux were shown tohave delayed sleep onset and more nighttime awakeningscompared to population norms.43 Sleep disorders were found to bemore frequent in children who suffered from colic during earlyinfancy in a prospective longitudinal study44 whereas anotherstudy did not find any persistent sleep problems in infants withcolic.45 However, it is not possible to separate the influence of thecondition and that of the parental response in the latter study onthe persistence of sleep problems.

Finally, children with neurodevelopmental disorders, such asautism, attention-deficit hyperactivity disorder, Tourette syndrome,and genetic syndromes leading to mental retardation, are alsoknown to be prone to sleep disorders.46 These take the form ofsevere difficulties falling asleep, frequent night awakenings, earlyawakenings in the morning. These can be due to the condition itselfand the medication used to treat it.

Parental characteristics

Parental characteristics may also impede or foster sleepconsolidation. Anxious, overprotective, depressive, and insecuremothers have infants with sleep problems in a greaterpercentage.47 Depression has been more extensively studied, andassociated with poor sleep consolidation in children.27,28,35 Onepossible mechanism is that mood disturbance in the mother leadsto an over-protectiveness that, in turn, interferes with the devel-opment of infant sleep autonomy.47 However, these studies do nottake into account the mother’s behaviors surrounding the child’ssleep period. On the other hand, the mother’s age and education

seem to have little influence on infant sleep consolidation.30 Ina representative population-based study,41 no parental character-istics (mother’s immigrant status, depression, over-protectiveness,or feeling of efficacy) were highly associated with poor sleepconsolidation, independently of the behaviors adopted around thechild’s sleep period.

The following factors have been found to be highly associatedwith poor sleep consolidation in early childhood.

Parental behaviors surrounding sleep onset

A longitudinal study showed that specific parental behaviors,such as parental presence during sleep onset and transfer of thechild to the parental bed in response to a nocturnal awakening,are the best predictors of sleep problems in early childhood.41

Parents that remain present until the child falls asleep or put theirchild to bed already asleep prevent him from learning to fallasleep on his own. Consequently, if the child wakes up during thenight, he will most likely experience more difficulty returning tosleep by himself. Knowledge transfer48 is defined as the capacityto perform something learned in one situation (e.g., falling asleepat sleep onset: initial context) in another situation (e.g., fallingasleep after nocturnal awakening if the child has no specificneeds). In order to train the child to fall asleep on his own,treatment should include modification of parental behaviors atbedtime. Behavioral interventions, which involve the parents, areeffective in treating a majority of early childhood dyssomniacases.49 In sum, resolving the child’s sleep problems improves thefamily’s quality of life.49

Parental behaviors in response to nocturnal awakening

An extensive population-based study found that specificparental behaviors in response to nocturnal awakening wereassociated with sleep fragmentation.41 For example, feeding thechild after nocturnal awakening was strongly associated withsleeping less than 6 consecutive hours per night at 5 months of age.However, this behavior is normal in unweaned children. One studyshows that unweaned children have shorter nighttime sleepperiods compared to weaned children.50 Feeding the child whennocturnal awakening no longer fulfills a physiological need couldimpede sleep consolidation. Moreover, comforting the child outsidehis bed (instead of in his bed) after an awakening is significantlyassociated with sleep fragmentation in early childhood.41 Com-forting the child outside his bed interferes with the development ofautonomous sleep habits, such as self-soothing in order to fallasleep alone after nocturnal awakening.

Breastfeeding: a controversial issue

Breastfeeding (vs bottle-feeding) has been associated with notsleeping at least 6 consecutive hours per night at the age of 5months.41 Some studies35,50 have also found a link betweenbreastfeeding and signaled nocturnal awakenings, whereas otherstudies found no such relationship.51,52 On the one hand, thisassociation could be explained by the fact that maternal milk ismore rapidly digested than formula milk, leading to shorter satietyperiods.53 On the other hand, one study observed that breast-fedinfants could be ‘‘good sleepers’’ if the mother increased the delaybetween the infant’s need and her response (the same delay as forbottle-fed infants, i.e. bottle preparation time).54 However, thevalue of breastfeeding should not be questioned, since it provideswell-documented positive benefits to both mother and child, and itfosters a strong mother–child bond.

E. Touchette et al. / Sleep Medicine Reviews 13 (2009) 355–361358

Cosleeping: an irregular sleep habit?

In Western cultures, sleeping alone is considered a milestone inthe process of getting a good sleep.22 Indeed, cosleeping, or sharinga room with another family member, has been associated withsleeping less than 6 consecutive hours per night in early childhood,when a variety of factors are considered simultaneously.41 Sleepingin the parental bed in response to nocturnal awakening has beenassociated with more sleep problems, specifically in children olderthan 4 years.5,55 The majority of children with a sleep problem hadslept in the parental bed after a nocturnal awakening (70%compared to 23% of children without sleep problems).55 Again,cause and effect are difficult to distinguish. Cosleeping in responseto nocturnal awakenings increased the occurrence of sleep prob-lems, whereas regular cosleeping was not detrimental to sleepquality.55 In fact, associations between cosleeping and sleep prob-lems are not reported in non-Western cultures.56 This might beexplained by the fact that, in non-Western cultures, cosleeping isnot reactive to nocturnal awakenings, but is instead a regularsleeping arrangement.

Familial, environmental, and cultural risk factors

There are major discrepancies in the findings on the impacts offamilial and cultural factors on infant sleep consolidation. Anepidemiological study in children aged 8–9 years revealed thatthose living in a modified family structure (e.g., single-parent orrecombined family) were at greater risk for sleep problems.57 Onthe other hand, several other studies have shown that familystructure has little influence on the consolidation of the sleep-wakerhythm in infants.42 Socioeconomic status and ethnicity may beassumed to influence the child’s sleep consolidation. Workingmothers reported more nocturnal awakenings by their childrenthan stay-at-home mothers.58 However, in our representativepopulation-based study,41 no familial (number of siblings, familystructure), environmental (income status), or cultural (immigrantstatus) characteristics were highly associated with poor sleepconsolidation, independently of parental behaviors, when multiplefactors were considered simultaneously.

Consequences of short sleep duration

Do sleep problems have negative consequences on the child’sdevelopment? Poor sleepers go to bed 1 h later on average, andtherefore sleep 1 h less than good sleepers.42 As the child grows up,it becomes imperative to assess the relationship betweennocturnal sleep duration and the potential consequences fordevelopment.

Behavioral functioning

There is much evidence that sleep problems are linked todaytime behavioral problems.1,2 Short sleep duration is associatedwith sleepiness in children and adolescents,59 and a wide range ofsleepiness behaviors has been reported in young children, fromclassical sleepiness symptoms (e.g., yawning) to hyperactive andimpulsive behaviors.1

Subjective studies suggest that sleep disturbances may beassociated with attention-deficit hyperactivity disorder (ADHD) inchildren.60,61 Conversely, the sleep architecture of children withADHD measured in the laboratory was found to be normal,62 butthese children had more bad than good nights63 and moved moreduring the night.62 In a longitudinal study, children with shortnocturnal sleep duration before age 3.5 years were found atincreased risk (2.5 times) for high hyperactivity–impulsivity scores

at 6 years compared to children with 11 h of sleep per night, evenafter controlling for potentially confounding variables.2 How couldshort sleep duration in early childhood lead to a hyperactivity–impulsivity problem later in life? One possible explanation is thatearly sleep deprivation interferes with the development of theneuronal systems that control daytime vigilance, particularly thehypocretin neurons located in the lateral hypothalamus. Paradox-ically, decreased vigilance may be expressed as agitation orimpulsive behaviors in young children.1

Cognitive functioning

The relationships between sleep duration at night, learningcapacity, and academic performance are well documented64. Ithas been reported that children with difficulties in recallingmaterial learned on the previous night have more unstablebedtimes and shorter sleep durations compared to children withno memory difficulties.64 A sleep laboratory study found that a 1-h increase in sleep duration for 3 consecutive nights producedbetter cognitive results in children with a mean age of 10.6years.65

In a longitudinal study, children with short nocturnal sleepduration across early childhood were at 3.2 times the risk forachieving low scores on the Peabody Picture Vocabulary test at theage of 5 years, and at 2.1 times the risk for low performances on theBlock Design subtest of the Wechsler Intelligence Scale for Children(WISC-III) at age 6 years, compared to children who had 11 h ofsleep per night in early childhood, even after controlling forpotentially confounding variables.2 These results suggest that shortsleep duration may decrease the child’s potential to achieveoptimal academic results and school adaptation.

Physical development

The prevalence of excess weight/obesity increased 2- to 4-foldover the past 2 decades.66 Concurrently, a decrease in nocturnalsleep duration has been observed in children. An approximate 40-min decrease in sleep duration in 2- to 8-year-old children wasreported across 3 longitudinal cohorts (1974, 1979, and 1986),largely due to later bedtimes.3 In our longitudinal study, we foundthat short sleep duration across early childhood increased byalmost 3 times the risk for overweight or obesity at 6 yearscompared to children who slept around 11 h per night,67 even aftercontrolling for potentially confounding variables and adjusted onweight at 2.5 years of age. Another longitudinal study68 had foundalso that short sleep duration increased the risk for obesity inschool-aged children but the sleep duration was not analyzed ina longitudinal way.

The biological mechanisms underlying this association are stillunknown. However, several explanations have been proposed. Adecrease in sleep duration influences the secretion of 2 keyhormones that regulate appetite.69 Sleep restriction leads toincreased ghrelin secretion (a peptide secreted by the stomach thatstimulates food intake and lipid storage) and decreased leptinsecretion (a hormone secreted by adipocytes that signals energybalance status to the hypothalamus). A high ghrelin-to-leptin ratiois known to stimulate appetite, which potentially leads to weightgain. Another possible explanation is that long sleep durationstimulates the secretion of growth hormone by the hypothalamus–pituitary–adrenal axis during slow-wave sleep, which reduces therisk of obesity. These mechanisms could also be related, becausea low secretion of ghrelin stimulates slow-wave sleep, therebyincreasing the secretion of growth hormone.69 On the other hand,a high level of ghrelin disturbs sleep due to hunger, thus reducing

Fig. 1. An integrative model of main factors and potential consequences (grey areas) associated with dyssomnias (sleep fragmentation or short sleep duration). The asteriskindicates that organic and neurodevelopmental disorders have not been studied in the context of a multifactorial analysis but play a role in dyssomnias.

E. Touchette et al. / Sleep Medicine Reviews 13 (2009) 355–361 359

the secretion of growth hormone, which potentially leads to weightgain.69

An integrative model of the risk factors and consequences ofdyssomnias

A theoretical model of infant sleep regulation integratingmultiple environmental systems was developed in 1993.32 Arevised model based on empirical data is proposed here (see Fig. 1).

It relies heavily on a series of analyses2,41,67,70 performed ona representative sample of children born in the province of Quebec(Canada) in 1997–1998 studied prospectively and longitudinally.This study allowed investigating several spheres of child develop-ment simultaneously in order to distinguish variables that arestrongly associated with poor sleep and also looking at the variousoutcomes of short sleep duration.

The proposed model first presents the factors most highlyassociated with poor sleep, with a variety of factors enteredsimultaneously into a logistic regression. This integrative modelsuggests that, among the many possible sources of sleep frag-mentation and short sleep duration, specific parental behaviorsaround the child’s sleep period (highlighted in grey) are the maincontributors to the development of childhood dyssomnias, inchildren without a neurodevelopmental or organic disorder. Thatis why behavioral treatments that also address sleep-relatedparental behaviors succeed in almost 90% of cases.49 Of course, thesleep behaviors are influenced by the parents’ personality traits(over-protectiveness, depression, etc.) and their child’s character-istics (especially a difficult temperament), both of which are inturn influenced by culture, socioeconomic status, and familystructure. However, factors such as the child’s sex and prematurity,

mother’s age and education, mother’s depression and feeling ofefficacy or over-protectiveness, use of a transitional object, incomestatus, and family type do not seem to be strongly associated withconsolidated sleep, in a way that is independent of parentalbehaviors.

Second, this model highlights the serious potential conse-quences of a modest but chronic loss of sleep in childhood . At leastthree developmental domains could be directly affected: behav-ioral/social adequacy, cognitive performance, and body weight. Insum, children with short nocturnal sleep in early childhood are atincreased risk for having high hyperactivity–impulsivity scores, lowperformance on cognitive tests, and overweight/obesity at the ageof 6 years.2,67

Conclusions

This review stresses the importance of allowing youngchildren to sleep at least 10 h per night, as suggested by theNational Sleep Foundation Poll71 for optimal general childhooddevelopment. It would be important to more accurately deter-mine the minimum required sleep duration threshold in earlychildhood. We should keep in mind that the required sleepduration may show inter-individual variation (short- and long-sleepers). To avoid childhood dyssomnias, one recommendationto parents is to foster the development of autonomous sleephabits by putting their child to bed in a drowsy but awakestate and letting the child fall asleep without parentalintervention.

Neurodevelopmental and organic disorders have not beenproperly studied in the context of a multifactorial analysis andshould be the object of further research.

Practice points

1. Prevention programs should focus on educating parentsabout normal sleep and dyssomnias in early childhood.

2. Pediatricians and clinicians should give sufficientattention to infant dyssomnias and promote giving thechild the opportunity to sleep at least 10 h per night assuggested by the National Sleep Foundation Poll.

3. When dyssomnias are reported in children, behavioralapproaches that address the modifications of parentalbehaviors surrounding sleep periods should beencouraged.

4. Clinicians should assess sleep habits among cases ofsuspected ADHD to eliminate the possibility of a falsediagnosis.

5. Clinicians should give strong recommendations to geta good night sleep, in addition to promoting morephysical exercise, in order to tackle the epidemicproblem of excessive weight and obesity.

Research agenda

1. More research is needed to investigate mediated asso-ciations between each risk factor and dyssomnias.

2. There is a need to objectively compare physiologicalsensory thresholds in good and poor sleepers to shedlight on the relationships between temperament andinfant dyssomnias.

3. Future studies should investigate the contribution ofgenetics to childhood dyssomnias and its associationwith the factors identified in the proposed model.

4. More longitudinal studies should examine whether theconsequences of short sleep duration are independentof each other, or to what extent they interact to producea more complex predicament.

5. Further investigations of academic performancethroughout elementary school and of cognitive/psychomotor functioning that involved executive func-tions, which are known to be under the control of thefrontal lobe and thus affected by sleep reduction, areneeded.

6. Experimental studies are needed to further explore therelationship between sleep and appetite. Homeostaticand circadian sleep control mechanisms may beinvolved, since they are linked to glucose metabolism,cortisol, and hypocretin secretion.

7. Future longitudinal studies should assess the effects ofearly treatment of dyssomnias on child development.

E. Touchette et al. / Sleep Medicine Reviews 13 (2009) 355–361360

Acknowledgements

This research was supported by a postdoctoral fellowship (E.Touchette) from the Canadian Institutes of Health Research.

References

*1. Dahl RE. The impact of inadequate sleep on children’s daytime cognitivefunction. Semin Pediatr Neurol 1996;3:44–50.

*2. Touchette E, Petit D, Seguin JR, Boivin M, Tremblay RE, Montplaisir JY. Asso-ciations between sleep duration patterns and behavioral/cognitive functioningat school entry. Sleep 2007;30:1213–1219.

* The most important references are denoted by an asterisk.

*3. Iglowstein I, Jenni OG, Molinari L, Largo RH. Sleep duration from infancy toadolescence: reference values and generational trends. Pediatrics2003;111:302–307.

4. Weissbluth M. Naps in children: 6 months-7 years. Sleep 1995;18:82–87.5. Ottaviano S, Giannotti F, Cortesi F, Bruni O, Ottaviano C. Sleep characteristics in

healthy children from birth to 6 years of age in the urban area of Rome. Sleep1996;19:1–3.

6. Anders T, Keener M. Developmental course of nighttime sleep-wake patternsin full- term and pre-term infants during the first year of life. Sleep1985;8:193–206.

*7. Thorleifsdottir B, Bjornsson JK, Benediktsdottir B, Gislason Th,Kristbjarnarson H. Sleep and sleep habits from childhood to young adulthoodover a 10-year period. J Psychosom Res 2002;53:529–537.

8. Acebo C, Sadeh A, Seifer R, Tzischinsky O, Hafer A, Carskadon MA. Sleep/wakepatterns derived from activity monitoring and maternal report for healthy 1-to 5-year-old children. Sleep 2005;28:1568–1577.

9. Borbely AA. A two-process model of sleep regulation. Hum Neurobiol1982;1:195–204.

10. Dunlap JC, Loros JJ, DeCoursey PJ. Chronobiology: biological timekeeping. Sun-derland, Mass: Sinauer Associates; 2004.

11. Swaab DF, Hofman MA, Honnebier MB. Development of vasopressin neuronsin the human suprachiasmatic nucleus in relation to birth. Brain Res Dev BrainRes 1990;52:289–293.

12. Vitaterna MH, Pinto LH, Turek FW. Molecular genetic basis for mammaliancircadian rhythms. In: Mh Kryger, Roth T, Dement WC, editors. Principles andpractice of sleep medicine. Philadelphia: Elsevier Saunders; 2005. p. 363–374.

13. Rivkees SA. Emergence and influences of circadian rhythmicity in infants. ClinPerinatol 2004;31:217–228.

14. Rivkees SA. Developing circadian rhythmicity in infants. Pediatrics2003;112:373–381.

15. McGraw K, Hoffmann R, Harker C, Herman JH. The development of circadianrhythms in a human infant. Sleep 1999;22:303–310.

16. Salzarulo P, Fagioli I. Post-natal development of sleep organization in man:speculations on the emergence of the ‘‘S process’’. Clin Neurophysiol1992;22:107–115.

17. Jenni OG. Sleep-wake processes play a key role in early infant crying. BehavBrain Sci 2004;27:464–465.

*18. Jenni OG, LeBourgeois MK. Understanding sleep-wake behavior and sleepdisorders in children: the value of a model. Curr Opin Psychiatry 2006;19:282–287.

19. Dijk DJ, Czeisler CA. Paradoxical timing of the circadian rhythm of sleeppropensity serves to consolidate sleep and wakefulness in humans. NeurosciLett 1994;166:63–68.

20. Carskadon MA, Vieira C, Acebo C. Association between puberty and delayedphase preference. Sleep 1993;16:258–262.

21. Touchette E, Mongrain V, Petit D, Tremblay RE, Montplaisir JY. Development ofsleep-wake schedules during childhood and relationships with sleep duration.Arch Pediatr Adolesc Med 2008;162:343–349.

22. American Psychiatric Association. Diagnostic and statistical manual of mentaldisorders. 4th ed.. Washington: American Psychiatric Association; 1994.

*23. Gaylor E, Goodlin-Jones B, Anders T. Classification of young children’s sleepproblems: a pilot study. J Am Acad Child Adolesc Psychiatry 2001;40:61–67.

24. Sadeh A, Lavie P, Scher A, Tirosh E, Epstein R. Actigraphic home monitoring ofsleep-disturbed and control infants and young children: a new method forpediatric assessment of sleep-wake patterns. Pediatrics 1991;87:494–499.

25. Louis J. Maturation du sommeil pendant les deux premieres annees de vie:aspects quantitatif, structurel et circadien. Neurophysiol Clin 1998;28:477–491.

26. Hoppenbrouwers T, Hodgman JE, Arakawa K, Geidel SA, Sterman MB. Sleepand waking states in infancy: normative studies. Sleep 1988;11:387–401.

27. Anders TF, Halpern L, Hua J. Sleeping through the night: a developmentalperspective. Pediatrics 1992;90:554–560.

28. Goodlin-Jones BL, Eiben LA, Anders TF. Maternal well-being and sleep-wakebehaviors in infants: an intervention using maternal odor. Infant Ment Health J1997;18:378–393.

29. Beltramini AU, Hertzig ME. Sleep and bedtime behavior in preschool-agedchildren. Pediatrics 1983;71:153–158.

30. Moore T, Ucko LE. Night waking in early infancy, I. Arch Dis Child 1957;32:333–342.

31. Keener MA, Zeanah CH, Anders TF. Infant temperament, sleep organization,and nighttime parental interventions. Pediatrics 1988;81:762–771.

32. Sadeh A, Anders T. Infant sleep problems: origins, assessment, interventions.Infant Ment Health J 1993;14:17–34.

33. Jenni OG, O’Connor BB. Children’s sleep: an interplay between culture andbiology. Pediatrics 2005;115:204–216.

34. Watson NF, Goldberg J, Arguelles L, Buchwald D. Genetic and environmentalinfluences on insomnia, daytime sleepiness, and obesity in twins. Sleep2006;29:645–649.

35. Zuckerman B, Stevenson J, Bailey V. Sleep problems in early childhood:continuities, predictive factors, and behavioral correlates. Pediatrics1987;80:664–671.

36. Oberklaid F, Prior M, Sanson A. Temperament of preterm versus full-terminfants. J Dev Behav Pediatr 1986;7:159–162.

37. Wolke D, Sohne B, Riegel K, Ohrt B, Osterlund K. An epidemiologic longitudinalstudy of sleeping problems and feeding experience of preterm and term

E. Touchette et al. / Sleep Medicine Reviews 13 (2009) 355–361 361

children in southern Finland: comparison with a southern German populationsample. J Pediatr 1998;133:224–231.

38. Rosen CL, Larkin EK, Kirchner HL, Emancipator JL, Bivins SF, Surovec SA, et al.Prevalence and risk factors for sleep-disordered breathing in 8- to 11-year-oldchildren: association with race and prematurity. J Pediatr 2003;142:383–389.

39. Scher A. A longitudinal study of night waking in the first year. Child CareHealth Dev 1991;18:701–711.

40. Carey WB. Night waking and temperament in infancy. J Pediatr 1974;84:756–758.

*41. Touchette E, Petit D, Paquet J, Boivin M, Japel C, Tremblay RE, et al. Factorsassociated with fragmented sleep at night across early childhood. Arch PediatrAdolesc Med 2005;159:242–249.

42. Minde K, Popiel K, Leos N, Falkner S, Parker K, Handley-Derry M. The evalu-ation and treatment of sleep disturbances in young children. J Child PsycholPsychiatry 1993;34:521–533.

43. Ghaem M, Armstrong KL, Trocki O, Cleghorn GJ, Patrick MK, Shepherd RW. Thesleep patterns of infants and young children with gastro-oesophageal reflux.J Paediatr Child Health 1998;34:160–163.

44. Savino F, Castagno E, Bretto R, Brondello C, Palumeri E, Oggero R. Aprospective 10-year study on children who had severe infantile colic. ActaPaediatr Suppl 2005;94:129–132.

45. Wake M, Morton-Allen E, Poulakis Z, Hiscock H, Gallagher S, Oberklaid F.Prevalence, stability, and outcomes of cry-fuss and sleep problems in the first2 years of life: prospective community-based study. Pediatrics 2006;117:836–842.

46. Hoban TF. Sleeplessness in children with neurodevelopmental disorders.Epidemiology and management. CNS Drugs 2000;14:11–22.

47. Paret I. Night waking and its relation to mother-infant interaction in nine-month-old infants. In: Call JD, Galenson E, Tyson RL, editors. Frontiers of infantpsychiatry. New York: Basic Books; 1983.

48. Ausubel DP, Robinson FG. School learning, an introduction to educationalpsychology. New York: Holt, Rinehart and Winston Montreal; 1969.

49. Richman N, Douglas J, Hunt H, Lansdown R, Levere R. Behavioural methods inthe treatment of sleep disorders-a pilot study. J Child Psychol Psychiatry1985;26:581–590.

50. Elias MF, Nicolson NA, Bora C, Johnston J. Sleep/wake patterns of breast-fedinfants in the first 2 years of life. Pediatrics 1986;77:322–329.

51. Adair R, Bauchner H, Philipp B, Levenson S, Zuckerman B. Night waking duringinfancy: role of parental presence at bedtime. Pediatrics 1990;87:500–504.

52. Kahn A, Mozin MJ, Rebuffat E, Sottiaux M, Muller MF. Milk intolerance inchildren with persistent sleeplessness: a prospective double-blind crossoverevaluation. Pediatrics 1989;84:595–603.

53. Burness NA. Infant feeding. In: Vaughan VC, McKay RJ, Behrman RE, editors.Nelson textbook of pediatrics. Philadelphia: WB Saunders; 1979.

54. Pinilla T, Birch LL. Help me make it through the night: behavioural entrain-ment of breast-fed infants’ sleep patterns. Pediatrics 1993;91:436–444.

55. Lozoff B, Askew GL, Wolf AW. Cosleeping and early childhood sleep problems:effects of ethnicity and socioeconomic status. J Dev Behav Pediatr 1996;17:9–15.

56. Morelli G, Rogoff B, Oppenheim D, Goldsmith D. Cultural variation in infants’sleeping arrangements: questions of independence. Dev Psychol 1992;28:604–613.

57. Paavonen EJ, Aronen ET, Moilanen I, Piha J, Rasanen E, Tamminen T, et al. Sleepproblems of school-aged children: a complementary view. Acta Paediatr2000;89:223–228.

58. Van Tassel EB. The relative influence of child and environmental character-istics on sleep disturbances in the first and second years of life. J Dev BehavPediatr 1985;6:81–86.

*59. Fallone G, Owens J, Deane J. Sleepiness in children and adolescents: clinicalimplications. Sleep Med Rev 2002;6:287–306.

60. Chervin RD, Dillon JE, Bassetti C, Ganoczy DA, Pituch KJ. Symptoms of sleepdisorders, inattention, and hyperactivity in children. Sleep 1997;20:1185–1192.

61. Lavigne JV, Arend R, Rosenbaum D, Smith A, Weissbluth M, Binns HJ, et al.Sleep and behavior problems among preschoolers. J Dev Behav Pediatr1999;20:164–169.

62. Konofal E, Lecendreux M, Bøuvard MP, Mouren-Simeoni MC. High levels ofnocturnal activity in children with attention-deficit hyperactivity disorder:a video analysis. Psychiatry Clin Neurosci 2001;55:97–103.

63. Gruber R, Sadeh A, Raviv A. Instability of sleep patterns in children withattention-deficit/hyperactivity disorder. J Am Acad Child Adolesc Psychiatry2000;39:495–501.

64. Curcio G, Ferrara M, De Gennaro L. Sleep loss, learning capacity and academicperformance. Sleep Med Rev 2006;10:323–337.

65. Sadeh A, Gruber R, Raviv A. The effects of sleep restriction and extension onschool-age children: what a difference an hour makes. Child Dev2003;74:444–455.

66. Ebbeling CB, Pawlak DB, Lubwig DS. Childhood obesity: public-health crisis,common sense cure. Lancet 2002;360:473–482.

*67. Touchette E, Petit D, Tremblay RE, Boivin M, Montplaisir JY. Associationsbetween sleep duration patterns and overweight/obesity at age 6. Sleep2008;31:1507–1514.

*68. Reilly JJ, Armstrong J, Dorosty AR, Emmett PM, Ness A, Rogers I, et al. Early liferisk factors for obesity in childhood: cohort study. BMJ 2005;330:1357.

69. Schussler P, Uhr M, Ising M, Weikel JC, Schmid DA, Held K, et al. Nocturnalghrelin, ACTH, GH and cortisol secretion after sleep deprivation in humans.Psychoneuroendocrinology 2006;31:915–923.

70. Petit D, Touchette E, Tremblay RE, Boivin M, Montplaisir J. Dyssomnias andparasomnias in early childhood. Pediatrics 2007;119:e1016–1025.

71. Mindell JA. Sleep in America. SRS Bulletin 2004;10:14–15.