Pediatrics 2012 Malow S106 24

A Practice Pathway for the Identification, Evaluation, and Management ofInsomnia in Children and Adolescents With Autism Spectrum Disorders

Beth A. Malow, Kelly Byars, Kyle Johnson, Shelly Weiss, Pilar Bernal, Suzanne E.Goldman, Rebecca Panzer, Daniel L. Coury and Dan G. Glaze

Pediatrics 2012;130;S106DOI: 10.1542/peds.2012-0900I

The online version of this article, along with updated information and services, islocated on the World Wide Web at:

http://pediatrics.aappublications.org/content/130/Supplement_2/S106.full.html

PEDIATRICS is the official journal of the American Academy of Pediatrics. A monthlypublication, it has been published continuously since 1948. PEDIATRICS is owned,published, and trademarked by the American Academy of Pediatrics, 141 Northwest PointBoulevard, Elk Grove Village, Illinois, 60007. Copyright © 2012 by the American Academyof Pediatrics. All rights reserved. Print ISSN: 0031-4005. Online ISSN: 1098-4275.

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A Practice Pathway for the Identification, Evaluation, andManagement of Insomnia in Children and AdolescentsWith Autism Spectrum Disorders

abstractOBJECTIVE: This report describes the development of a practice

path-

way for the identification, evaluation, and management of insomnia inchildren and adolescents who have autism spectrum disorders (ASDs).

METHODS: The Sleep Committee of the Autism Treatment Net

work(ATN) developed a practice pathway, based on expert consensus, tocapture best practices for an overarching approach to insomnia bya general pediatrician, primary care provider, or autism medical spe-cialist, including identification, evaluation, and management. A fieldtest at 4 ATN sites was used to evaluate the pathway. In addition, a sys-tematic literature review and grading of evidence provided dataregarding treatments of insomnia in children who have neurodevelop-mental disabilities.

RESULTS: The literature review revealed that current

treatments forinsomnia in children who have ASD show promise for behavioral/educational interventions and melatonin trials. However, there isa paucity of evidence, supporting the need for additional research.Consensus among the ATN sleep medicine committee expertsincluded: (1) all children who have ASD should be screened forinsomnia; (2) screening should be done for potential contributingfactors, including other medical problems; (3) the need fortherapeutic intervention should be determined; (4) therapeuticinterventions should begin with parent education in the use ofbehavioral approaches as a first-line approach; (5) pharmacologic

therapy may be indicated in certain situations; and (6) there shouldbe follow-up after any intervention to evaluate effectiveness andtolerance of the therapy. Field testing of the practice pathway byautism medical specialists allowed for refinement of the practicepathway.

CONCLUSIONS: The insomnia practice pathway

may help health careproviders to identify and manage insomnia symptoms in children and

AUTHORS: Beth A. Malow, MD, MS,a,b,c Kelly Byars, PsyD,dKyle Johnson, MD,e Shelly Weiss, MD,f Pilar Bernal, MD,a,cSuzanne E. Goldman, PhD,g Rebecca Panzer, MA, RD, LD,hDaniel L. Coury, MD,i and Dan G. Glaze, MDj

Departments of aNeurology and bPediatrics and cKennedy Center,Vanderbilt University Medical Center, Nashville, Tennessee;dDepartment of Pediatrics, University of Cincinnati College ofMedicine, Cincinnati Hospital Children’s Medical Center,Cincinnati, Ohio; eDepartment of Psychiatry, Oregon Health andScience University, Portland, Oregon; fHolland Bloorview KidsRehabilitation Hospital, Toronto, Ontario, Canada; gKaiserPermanente Northern, San Jose, California; hMassGeneralHospital for Children, Boston, Massachusetts; iDepartment ofPediatrics, Nationwide Children’s Hospital, Columbus, Ohio; andjDepartments of Neurology and Pediatrics, Baylor College ofMedicine, Houston, Texas

KEY WORDSactigraphy, education, sleep, sleep latency

ABBREVIATIONS

ASD—autism spectrum disorderATN—Autism Treatment NetworkCSHQ—Children’s Sleep Habits QuestionnaireNICHQ—National Initiative for Children’s Healthcare QualityRCT—randomized controlled trial

This manuscript has been read and approved by all authors.This paper is unique and not under consideration by any otherpublication and has not been published elsewhere.

www.pediatrics.org/cgi/doi/10.1542/peds.2012-0900I

doi:10.1542/peds.2012-0900I

Accepted for publication Aug 8, 2012

Address correspondence to Beth Malow, MD, MS, Burry Chair inCognitive Childhood Development, Director, Vanderbilt SleepDisorders Division, 1161 21st Avenue South, Room A-0116,Nashville, TN 37232. E-mail: [email protected]

PEDIATRICS (ISSN Numbers: Print, 0031-4005; Online, 1098-4275).

Copyright © 2012 by the American Academy of Pediatrics

FINANCIAL DISCLOSURE: The authors have indicated they haveno financial relationships relevant to this article to disclose.

adolescents who have ASD. It may also provide a framework to evaluatethe impact of contributing factors on insomnia and to test the effec-tiveness of nonpharmacologic and pharmacologic treatment strategiesfor the nighttime symptoms and daytime functioning and quality of lifein ASD. Pediatrics 2012;130:S106–S124

S106 MALOW et alDownloaded from pediatrics.aappublications.org at Indonesia:AAP Sponsored on November 12, 2012

SUPPLEMENT ARTICLE

Approximately 1 in 110 children fu

lfillsthe Diagnostic and Statistical Manualof Mental Disorders, Fourth Edition,Text Revision, diagnostic criteria forautismspectrum

disorders(ASDs)as defined by delayed or abnormalsocial interaction, language as used insocial communication, and/or restrictedrepetitive and

stereotyped patternsof behavior, interests, and activities.1

Children who have ASD are at greaterrisk for developing sleep problems than

typically developing children. Researchhas documented that the prevalence ofsleep disturbances ranges from 53% to78% for children who have ASD com-pared with 26% to 32% for typically de-veloping children.2,3

The key components of

pediatric in-somnia are repeated episodes of dif-ficulty initiating and/or maintainingsleep, including premature awaken-ings, leading to insufficient or poor-quality sleep. These episodes result infunctional impairment for the child or

other family members.4 In typicallydeveloping children, the primary causeof insomnia is behaviorally based.5 Inthe ASD population, however, insomniais multifactorial. It includes not onlybehavioral issues but also medical,neurologic, and psychiatric comorbid-ities; it is also an adverse effect of themedications used to treat symptoms ofautism and these comorbidities.6

Typically developing children

who haveinsomnia are at increased risk forneurobehavioral

mailto:[email protected]

problemssuch asimpairments in cognition, mood, atten-tion, and behavior.5,7–9 Similar to thebehavioral morbidity associated withpediatric insomnia that is observed inthe general population, children whohave ASD and sleep problems are proneto more severe comorbid behavioraldisturbances compared with childrenwithout sleep disturbances.10 In addition,treating insomnia in children who haveneurodevelopmental disorders may im-prove problematic daytime behaviors.11

Despite the prevalence of and

morbidityassociated with pediatric insomnia,there is evidence that sleep disorders inchildren often go undetected and un-treated.12–14 Medical practitioners of-ten do not ask about sleep concerns orparents do not seek assistance.15 Manyparents have poor knowledge aboutsleep development and sleep prob-lems.16 This is particularly relevant tochildren who have ASD, in that parentsmay present to the pediatrician withconcerns regarding aggression, im-pulsivity, inattention/hyperactivity, orother behavioral issues that may besecondary to a sleep disorder. Thecontribution of the sleep disorder maybe undetected due to emphasis ontreating the behavioral issue as op-posed to identifying and treating theunderlying factors. This deemphasis ofunderlying factors may be due to theabsence of a standardized approachfor recognition and treatment of in-somnia in children who have ASD.

Guidelines exist for sleep screening

andintervention in typically developingchildren.17,18 Guidelines and empiricalsupport also exist for the effectiven

essof behavioral treatment of bedtimeproblems and night wakings in chil-dren.18–21 Specific behavioral treat-ments supported include the following:unmodified extinction: leaving thechild’s bedroom after putting the childto bed and not returning until morningunless the child is ill or at risk for in-jury; extinction with parent presence:parent is present in the room with thechild but does not interact with himor her; graduated extinction: parentreturns to child’s bedroom to attendto child on request or agitation butincreases the time in between requestsby the child for the parent to return;preventive parent education: providingeducation to parent on sleep habitsand bedtime routine; bedtime fading:delaying bedtime to promote sleep andthen “fading” or advancing bedtime

once child is falling asleep easier; andscheduled awakenings: awakening thechild before a spontaneous awakening.Extinction and parent education havestrong empirical support whereas theother interventions are less confidentlysupported.18 To our knowledge, how-ever, there are no published guidelinesrelated to management of insomniain children who have ASD, includingscreening and treatment. The evidencethat children who have ASD are atgreater risk for insomnia and itsmorbidity suggests that sleep screen-ing in this population of children isextremely important. The ideal evalua-tion of insomnia in children who haveASD involves a comprehensive sleepassessment, as outlined in a recent

review.22

To facilitate the evaluation of childr

enwith ASD for insomnia, the Autism Treat-ment Network (ATN) in association withthe National Initiative for Children’sHealthcare Quality (NICHQ) worked col-laboratively to develop the clinicalpractice pathway presented in this arti-cle. The intention of this clinical practicepathway is to emphasize the need forscreening of sleep problems in ASD a

ndto provide a framework for decision-making related to best practices in thecare of children and adolescents withASD in primary care settings, when seenby a general pediatrician, primary careprovider, or autism medical specialist.The pathway is not intended to serve asthe sole source of guidance in the eval-uation of insomnia in children who haveASD or to replace clinical judgment, andit may not provide the only appropriateapproach to this challenge.

METHODS

Guideline Development

The ATN Sleep Committee consists ofpediatric sleep medicine specialists aswell as developmental pediatricians,neurologists, and psychiatrists. The

PEDIATRICS Volume 130, Supplement 2, November 2012 S107Downloaded from pediatrics.aappublications.org at Indonesia:AAP Sponsored on November 12, 2012

clinical practice pathway was designedto assist primary care providers andothers working directly with familiesaffected by ASD in addressing the chal-lenge of insomnia with regard to iden-tification, assessment, and management.

Insomnia was defined as

“repeateddifficulty with sleep initiation, duration,consolidation, or quality that occursdespite age-appropriate time and op-portunity for sleep that results in day-time functional impairment for thechild and/or family.”18 The responses ofthe parents to selected questions onthe Children’s Sleep Habits Question-

naire (CSHQ)23 identified those patientswho have insomnia.

After performing a systemi

c review ofthe literature, expert opinion and con-sensus was used to form the basis of thepractice pathway (Fig 1). The ATN SleepCommittee’s knowledge of the litera-ture and applicability to clinical prac-tice informed best practices, which inturn created an overarching approachto insomnia within ATN sites by theautism medical specialist.

Systematic Review of the Li

terature

We conducted a systemati

c literaturereview to find evidence regardingthe treatment of insomnia in children

diagnosed with ASD (questions andsearch terms available on request fromthe authors). We searched OVID, CINAHL,Embase, Database of Abstracts and Re-view Database of Abstracts of Reviewsand Effects, and the Cochrane Databaseof Systematic reviews databases, withsearches limited to primary and sec-ondary research conducted withhumans, published in the English lan-guage, involving children aged 0 to 18years, and published between January1995 and July 2010. Individual studieswere graded by using an adaptationof the GRADE system24 by 2 primaryreviewers and then reviewed by contentexperts for consensus. Discrepancieswere resolved by a third party.

Pilot Testing of the Pathway

The ATN selected 4 pilot sites (BaylorUniversity, Houston, Texas; OregonHealth and Science University, Portland,Oregon; Kaiser Permanente Northern,San Jose, California; University of Mis-souri, Columbia, Missouri) to test thefeasibility of the practice pathway andprovide information regarding neededmodifications. The pilot sites collecteddata to document adherence to the

practice pathway and participated inmonthly conference calls to provide

updates, understand variance, and re-commend changes. Working with theNICHQ, members of the ATN SleepCommittee refined and finalized thepractice pathway on the basis of feed-back from the pilot sites. In response torecommendations from the pilot sitesto increase feasibility, the NICHQ alsodeveloped a 1-page checklist designedto guide providers through the practice

pathway (Fig 2).

RESULTS

Results of the Literature Review

The search identified 1528 articles. Af-ter removing review articles, com-mentaries, case studies with fewer than10 subjects, studies that included chil-dren who did not have ASD, non-intervention trials, and articles thatdid not address our target questions,20 articles remained (Table 1). Wereviewed the literature for studies re-lated to other aspects of the practicepathway (eg, screening for insomnia,identifying comorbidities, importanceof follow-up) in the ASD populationand were unable to identify evidence-based reports for aspects other thantreatment. A comprehensive review25

and consensus statement26 relatedto the pharmacologic management of

FIGURE 1Checklist for carrying out the practice pathway in children who have ASD and insomnia. CSHQ, Children’s Sleep Habits Questionnaire.


SUPPLEMENT ARTICLE

FIGURE 2Practice pathway for insomnia in children who have ASD.


for6moto2y

treatm

en

tmg;oraltablet.Durati

on

andbehavioraldisord

ers

wakings)beforeandduri

ng

graduallyadvancedto

0.1

bedtime,latency,numb

erof

initialdose0.05mgan

dwithASD(NewJersey)andsle

ep

Caregiverreport(avera

ge

Included:19childrenaged4to16yClonidine1timeperd

ay,enceph

alopath

y d efinedcongenitaloracquir

ed

Excluded:childrennosographi

cally

(absenttoverysever

e)

hyperkinesi

a

earlywaking.Scored0to

4aggressiveness,a

nd

asleep,nightwakings,a

nd

ofseveremooddisorder

s,

disorders;di

fficultyfalling

withcontinuouspresence($

1y)

Evaluation(includedsl

eep

TIDfor60d

withASD(UniversityofBolog

na)

Included:25childrenaged2to20yNiaprazine1mg/

kgperdayBehavioralSummarized

Mingetal,200

846

control,levelII

IPre/post-no

Excluded:Notspec

ified

1506103d)

(meanduratio

n:

rangedfrom11to368

dmg).Treatm

entdurati

on

ofsleep(P=.002

)

interferingrepetitivebeha

vior

effects(range:7.5

–45

seenontheCGIseverityratin

gs

depression,insomnia,a

nd

symptomsandsi

de

sign

ificantimprovementwas

injury,irritability,anxi

ety,

onresponseoftarge

timprovedsleep.Statistic

ally

symptomsofaggression,s

elf-

individeddoses,bas

ed

nonresponders,3show

ed

alsoinclude

d

wasprescribedtotarg

et

maximumof45mgdai

lyshowedimprovedsleep.O

f17

assessingsleepqualityw

as

intellectualdisability.Mirtaza

pine

incrementsupto

aimproved).Fiveof9respond

ers

improvementite

m

(Indiana);20hadcomor

bid

increasesm

adein7.5-

mg

improvedorverymu

ch im

provement.Amod

ifiedCGI

adults,aged3to23ywithAS

D7.5mgdailywithdosa

ge

accordingtoaCGIscoreofm

uch

rateseverityan

d

Included:26childrenandyo

ung

MirtazapinestartingdoseofCliniciansusedtheCGIsc

aleto

Nineparticipantsresponded(d

efined

Wisconsin

)(Hemokinetics,Inc,Madi

son

TriTrac-

R3DErgometer

7-dsleepdiary

Handapraxiascal

e

Rossietal,199

945

control,levelII

IPre/post-no

Poseyetal,200

144

Excluded:NotspecifiedSF-36HealthSurvey

SyndromeRegist

er

recruitedfromAustralianR

ett

62femalesaged4to30

y8-wktrial;controlgroupinclude

d41y;recruitedfromprevio

us

SeverityInd

ex

twiceadayfor6mo

consistedof21femalesaged

7to

100mg/kgliquidL -

carnitineRettsyndromeSymptoms

Included:experimentalgr

oup

levelIII

Pre/post-control,

developmentaldisord

ers

andwakingsinchildrenwi

th

Clonidineimprovessleeplat

ency

stillexperiencednightwaki

ngs

experiencedimprovemen

ts;5

sleepmaintenancedisord

ers

duringtreatm

ent);16of17w

ith

beforetreatm

ent,0.5–

2h

improvedsleepinitiation(2–

5h

Sixteenof17childrenexperien

ced

ASD

nightwakingsinchildren

with

improvingsleeplatencya

nd

Niaprazineiseffective

in

bytheendofthetrial(P,.001)

improvementinsleepdisord

ers

Evaluationshow

ed

BehavioralSummari

zed

Comparedwithstartofthetreatm

ent,

childrenwithAS

Dimprovingsleepqualit

yin

Mirtazapineiseffective

in

Ellawayetal,200

143

syndrom

ewakingsinchildrenwithR

ett

sleep,ornumberofnig

ht

notduration,latency,day

time

improvessleepe

fficiencybut

supp

lementatio

nConclusions

Result

sConclusion

MeasuresUsedtoArrive

at

InterventionandDurat

ion

StudyandGrad

e

L- carnitine

ornightwakings(P=.25

)(P=.15),daytimesleep(P=.5

5),

duration(P=.57),laten

cy e fficiency(P,.03)butnot

sign

ificantlyimprovedsleep

controls,L-

carnitine

ComparedwithRettsyndro

me

Sampl

e

TABLE

1Continued

Excluded:notspec

ified

washou

tintravenously;

no

porcinesecreti

noflargerstudy(Californi

a)

intervention2CU/

kgwithautism

recruitedassubs

et

4wkplaceboand4wk

Included:17childrenaged3to

8y

individeddose

samaximumof3.5mg/

day

thentitratedt

ostartedat0.5mgnight

ly slowerdosing$45k

g

,20kg=similar,except

syndrome,and/

orweight,15kg

historyofneurolepticm

align

ant

previoustrialwithrisperido

ne,

sign

ificantm

edicalcondition,

gonadotropintestresultforgi

rls,

positiveb-

humanchorionic

maximumof2.5mg/

day

Excluded:Mentalage,18

mo,

20to44.9kg=0.5mgupt

o

RCT,levelII

I

Honomichletal,200

242RCT,levelI

I

NetworkwithAS

D

placeboorrisperido

ne

PediatricPsychopharm

acolog

y

6mo(responders)giv

en

fromResearchUnitso

n

Parentreportsleeplo

gIncluded:101childrenaged5to17y16wk(nonresponde

rs)to

Amanetal,200

541

interventions

Pharmacologic

StudyandGrad

e

TABLE

1ResultsofSystematicLiteratureReview

waking,m

orningris

e)

onset,time/

durationnight

Sleepdiary(bedtime,sle

ep

withASD

andnightwakingsinchildr

en

duration,bedtimeresista

nce,

improvesleep-

onsetdelay,

Secretindoesnotsign

ificantly

3–

7];post,m

ean:4.3[range:3–

8])

Sleepduration(Pre,m

ean:4.7[ra

nge:

3–

7];Post,m

ean:3.6[range:3–

5])

Nightwakings(Pre,m

ean:4.1[ra

nge:

[range:1–

3])

[range:1–

3];Post,m

ean:1.6

Sleep-

onsetdelay(Pre,m

ean:2.1

6–17];Post,m

ean:8[range:6–

13])

resistance(Pre,m

ean:9[ran

ge:

CSHQscores:Bedti

me

Secretindidnotsign

ificantlyaffect

CSH

Q

(parentreport

)mildorm

oderate/

severe

Adverseeventsscored

asM

ovementSca

le

Abnorm

alInvolunta

ry

ratesofadverseoutcom

es

butnotsleepduration;hi

gh

latencyinchildrenwithA

SD

Risperidoneimprovessl

eep

andconstipation(12%vs10

%)

di

fficultywaking(8%vs12%

),(10%vs33%),rhinitis(8%vs16

%),

(29%vs33%),excessiveapp

etite

somnolence(12%vs37%),enur

esis

versusrisperidone,respectiv

ely):

scoredasm

oderate(place

bo

6mo(29min).Adverseeve

nts

(17min;40min)butnotbeyo

nd

durationincreasedshort-

term

(P=.02;P=.05).Averagesle

ep

commoninrisperidonegro

up

Sleepproblemsandanxietyl

ess

Conclusions

Result

sConclusion


at


ion

Sam

ple


SUPPLEMENT ARTICLE


,4wk

takingsedativemedication

sfor

currentlyusingmelatoninan

d/or

Excluded:childrenpreviou

sly/

RCT,levelI

I

thelast6mo)

(UnitedKingdom)

awakening

)nightwaking4timesperweek

for

(atleast1hsleeplatencyand/

or

nightwakings,morni

ng

thenreversedfor4w

k

sleeptime,sleeplaten

cy,

for4wk,washout1wk

, withautism

andsleepingdi

fficulty

Parentalsleepcharts(tot

al

Placeboor5mgmelaton

inIncluded:7childrenaged4to1

6ysu

chasFragileXorRettsyndro

me

neurodevelopmentaldisorder

smedications,andthosewitho

ther

currentlyonpsychotro

pic

currentlyonmelatonin,th

ose

Sleepdi

fficultiesquestionnaire

Excluded:childrenpreviousl

yor

a1mowashout

moforeachagentwit

hTreatm

entphaselaste

d3

improvementof$50

%.

achieved,d

efinedasan

until“good”sleepw

as

psychotropicmedicatio

ns

amaximumdoseof10

mg

successfulandwerefree

of

nightsby2mgto

managementthatwas

not

bytheparentevery

3

Childrenhadundergonebeha

vior

Thedosewasincreas

ed

everymonthfor9m

o

and/

orreducedtotalsleeptime.

overtotheotheragen

t.timeawake)werecollect

ed

latency,excessivenightwa

king,

placeboandthencross

ed

sleeptime,nightwakin

gs,

withASDandprolongedsle

ep

beforeplannedsleep,

or

melatonintaken,bedti

me,

Included:20children,aged4to16yMelatonin2mg,30to40minDailysleepdiaries

(time

GarstangandWallis,200

627RCT,levelII

I

Wrightetal,201

149

[CI:9.68–

9.99])

8.75h[CI:8.56–

8.98];9.84h

baseline(8.05h[CI:7.65–

8.44];

Durationincreasedby1.79hver

sus [CI:0.04–

0.12])

[CI:0.20–

0.34];0.08

(0.35[CI:0.18–

0.53];0.26

pernightversusbaseli

ne

Wakingspernightdecreasedby0

.27 [CI:0.98–

1.13])

1.91h[CI:1.78–

2.03];1.06h

baseline(2.6h[CI:2.28–

2.93];

latencyimproved1.54hver

sus

valuesrespectively:Sl

eep

Baseline,placebo,andmelat

onin

wakingsandsleepdurati

on

latencynumberofnig

ht

treatm

enttoimprovesle

ep

Melatoninisaneffecti

ve

othersleepdisorde

rsparasomnia,sleepapnea

,or

treatm

ent(P=.04)butn

ot

Dyssomniasubscaleimproved

with

StudyandGrad

e

nightwaking

schildrenwithASDbutn

ot

latencyandtotalsleeptim

ein

Melatoninimprovessle

ep

Conclusions

Result

sConclusion


at


ion

notimprove(P=.2

)withplacebo.Nightwakings

did

melatonintreatm

entcomp

ared

longer(P=.002)durin

g(P=.004)andtotalsleeptimew

as

Meansleeplatencywaslow

er

Sampl

e

TABLE

1Continued

ferritin,transferri

n)

albumin,vitamin

B12,serum

Bloodsample(MCV,m

erc

ury,

powderedelementalir

on

microencapsulate

d

sign

ificantly(16to29mg/L)

DuringSleepScal

e60mg/

dayof

supp

lementatio

n

MeanferritinandMCVincreas

ed

PeriodicLegMoveme

nts

Ifnottolerated,receiv

ed

Excluded:currentlytakingi

ron

Scale(P=.82)

MovementsDuringSl

eep

(P=.83),orPeriodicLe

gwithferritin(P=.61),irritabili

tylatency;norelationwasfou

nd

35%hadimprovedsle

ep

(Toronto)

sign

ificantly(29%;P=.04)and

ferritinmeasuredpreviou

sly

scores,restlesssleepimpro

ved

Children

perdayfor8wk

diagnosedwithautism

wi

th

Perthesleepdisturbancesc

ale

SleepDisturbanceScale

for

6mgelementaliron/

kgIncluded:33childrenaged2to

5y

bodyweigh

tdailyintakeof3ml/

5lb

TIDwithfoodforatota

lSS-III;fulldose1ml/

5lb

Days50to90:continu

edtransitiontoSS-

III

Days35to50:gradu

al

vitaminC

) pyridoxamine,a2lipoica

cid,

B 6,pyridoxine,pyridox

al,

doseofSS-II

Excluded:notspecifiedDays25to34:heldmaximumBloodandurinesample(plasm

amultivitamin(Arizo

na)

thanstandardchildre

n’s

multivitaminsupplementso

ther

mo,andnoprevioususe

of

placebo(P=.03

)maximu

m

improvedcomparedw

ith

increasedlinearlyt

otreatm

enttherapiesinprevio

us2

withASDwithnochangesi

nasevidencedbyCGIsco

re(standardmultivitam

in),

Days0to24:1/8doseofSS-IICGISleepandgastrointestinalsymptoms


8y

Pre/post-

control,levelII

Dosm

anetal,200

748RCTlevelII

Excluded:notspec

ified

AdamsandHolloway,20

0447

Otherbiologicagen

ts

levelIII

casecontrol

,

Retrospectiv

e

StudyandGrad

e

TABLE

1Continued

movem

ent

slatency,orperiodicl

eg

affectirritability,sle

ep

childrenwithASDbutdoes

not

improvesrestlesssleep

in

Oralironsupplementati

onsc

oreinchildrenwithAS

DapositiveimpactonCGIsl

eep

vitaminC)m

ayha

ve

(includingvitamin

B6and

Moderate-

dosemultivitamin

Conclusions

Result

sConclusion


at


ion

Sampl

e


SUPPLEMENT ARTICLE


beforebedtim

e$30minon$3nightsperweek

phase:inertliquid30m

inwithASDandsleep-

onsetdelayof

Actigraphy;CS

HQ

Two-

weekacclim

ation


9y

aged.4y

upto6mginchildren

inchildrenaged,4yan

ddosetomaximumof4

mg

Physiciancouldincrea

se

.15minduringthenigh

tFRischildrenawokefo

r

Childrenadvisedtogive2

mg

Malowetal,201

152

medicationsfor6mopreviou

sly

conditions,and/

ortaking

belowcutoff,coexisti

ng

diagnosisbutwithCARSsco

re

Excluded:childrenwithauti

smPre/post-

control,levelII

(Italy)

before

5AM.3timesperweek)

weeknightwakings,andwak

ing

minsleeplatency,.3timesp

er

study

,29.5withsleepdisorder(.45

n=16,respectivel

y)

withautism

andCARSsco

re

Included:25childrenaged2.6to9.6y6-to24-

mo(n=25and

Giannottietal,200

651

tolerate

dwithASD.Itissafeandwel

lparentingstressinchildr

en

daytimebehaviora

nd

andimprovesaspects

of

treatm

entofsleeplaten

cy,


ve

timeorwaketimeaftersleepons

et P,.0001)butnottotalslee

psleeplatency(42.9to21.6

min;

improvementsweresee

nin

statisticallysign

ificant

withacclim

ationphas

e),

Withmelatonintreatm

ent(comp

ared

and2mgCR)

duration,daynap

s)beforebedtime(1mgF

R

duration,nightwakingsa

nd

melatonin30to40mi

n

Sleepdiary(bedtime,riseti

me,

3mgcontrolled-

release

StudyandGrad

e

ASD

resistanceinchildrenwi

thnightwakings,andbedti

me

duration,latency,numbe

rof

treatm

enttoimprovesle

ep


ve

Conclusions

Result

sConclusion


at


ion

P,.001)

years1and2(63vs44vs44

;improvementinCSHQscore

sin

showedsign

ificant

Thosewhocontinued24

mo

irregularityin61%

(P,.001).

63%

(P,.001),andbedtime

parentalpresenceatbedtim

ein

cosleepingin55%

(P,.001),

from70to10min(P,.001),

awaketimeaftersleeponset

by

indurationby2.6h(P,.001),

diariesshowedimprovem

ents

improved(P,.01).Slee

pdisorderedbreathingal

so improved(P,.001).Slee

p-

sleepinessweresign

ificantly

wakings,anddayti

me

resistance,anxiety,ni

ght

regardinglatency,durati

on,

vs43;P,.001).CSHQvalue

s weresign

ificantlyimproved(65

CSHQvaluesfrombaselineto6

mo

CSH

Q

Sampl

e

TABLE

1Continued

comorbidity

withmajorpsychiatr

icpsychotropicmedication

sor

Excluded:childrentak

ing

Pre/post-

control,LevelII

problemsinlast3mo(Helsink

i)syndromeandseveresle

ep

diagnosedwithAsperg

er’s

Included:15children5to1

7y

Paavonenetal,200

350

Excluded:notspec

ified

RCTlevelII

washout

)reversedfor2wk(n

oproblems(Californi

a)

bedtimefor2wk,the

nsyndromewhoreportedsle

ep

given30minbefor

ewithautism

and/

orFragileX

Included:18childrenaged2to15yPlaceboor3mgmelato

nin

Wirojananetal,200

928

StudyandGrad

e

TABLE

1Continued

Actigraph

yQuestionnair

e

Teacher’sD

aytimeSleepi

ness

KarolinskaSleepinessSc

ale

CBCL

Children

SleepDisturbanceScale

for

to480.48650.71;P=.57

2).

orduration(477.40655.

56

5.57to86.0364.62;P=.33

1)

foundinsleepe

fficiency(85.136

Nosign

ificantchangesw

ere

6.12to17.8566.25;P=.04

8).

numberofwakings(from15.1

46

9.64;P=.002)butincreas

ed

(from40.02624.09to21.82

64.99;P=.041)andsleeplate

ncy

activity(31.3967.86to18.7

46

Problem

s30minbeforebedfor1

4d

Melatoninimprovednoctu

rnal

Received3mgofm

elatoninChildren’sSelf-

ReportforSleep

Bend,Orego

n)

Actiwatch(PhilipsRespiron

ics,

(P=.73;effectsize:0.35

40)

0.07butwereinsign

ificant

awakeningsw

ereimprove

dby

effectsize:2.80),a

nd

improvedby42min(P=.01

7;

effectsize:1.79),sleepon

set

participantsby28min(P=.1

0;

improvedin11of1

2effectsize:2.12),sleeplate

ncy

participantsby21min(P=.05

7;

ofnightwakings

)

durationimprovedin9of1

2duration,sleeponset,nu

mber

Comparedwithplacebo,sl

eep

Sleepdiary(sleeplaten

cy,

syndrom

e childrenwithAsperge

r’s

sleepe

fficiency,ordurationin

latencybutnotnightwaki

ngs,

nocturnalactivityandsle

ep

treatm

enttoimpro

ve


ve

Conclusions

Result

sConclusion


at


ion

waking

ssleeponsettimebutnotni

ght

duration,sleeplatency,

and

treatm

enttoimprovesle

ep


ve

Sampl

e


SUPPLEMENT ARTICLE


nottobetakingmedicati

on

diagnosedwithASD,w

ere

withepilepsyand/

orif

Session1:goalsetti

ng

Excluded:excludedifdiagn

osed

(Australia

) perceivedsleepdi

fficulty

time)

(n=7)orASD(n=6)with

cosleeping,m

orningw

ake

follow-

upat3and12mo

eitherFragileXsyndro

me

weeklytelephoneca

lls;

13families)aged5ywit

hsleeponset,wakin

g,

Fivesessionsover7wkw

ithSleepDiary(behavior,light

sout,

Included:13children(acr

oss

concern

sindividualslee

p

Session3:addres

s

wakin

gandearlymornin

gminimizenightwaki

ng

waking

s

Latency,duration,ni

ght

Session2:Strategies

to

sleep

CSH

Qthatm

aycontributetodisord

ered

neurologic/

medicalconditions

routinebasedonFISHa

nd

habitsandabedtim

eapnea,narcolepsy,a

nd

sleepdisorderssuchassle

ep

daytimeandnightti

me

Session1:establish

ed

Excluded:childrenwithprim

ary

Actigraph

y

Caseseries,levelI

II

Weiskopetal,200

532

levelII

Pre/post-

nocontrol,

anissue

sleepbut50%stillconsideredsl

eep

100%ofparentsreportedimpro

ved

Durationwasvariableandunchan

ged

Nightwakingimprovedfor7of10(70

%)

addresse

d

Cosleepingwasal

soSession5:reviewsessi

onte

chniques

Session4:extincti

onsu

pportstrategi

es

instructionsandpartn

er

Session3:effecti

vere

presentation

reinforcementandvis

ual

interventionwi

thconsequences.Crea

ted

antecedentsa

nd

Session2:learningtheo

ry;

Sleeplatencyimprovedin6of10(60

%)im

provem

entand46.2%substant

ial

moderateimproveme

nt,

19.2%nochange,26.

9%

7.7%moderatedeteriorat

ion,

Baselinecomparedwith12

mo:improvem

entand41.3%substant

ial

moderateimproveme

nt,

27%nochange,23.

8%

4.8%moderatedeteriorat

ion,

1.6%substantialdeteriora

tion,

Baselinecomparedwith3

mo:improvem

ent

sand40.6%substant

ial

29.7%moderateimprove

ment,

sleepbehaviors,25%nocha

nge,

4.6%moderatedeteriorati

onof

Baselinecomparedwithinterven

tion:

developmentaldisabili

ties

notdurationinchildrenwit

hlatencyandnightwakings

but

parentsimprovedsle

ep

Educationalintervention

with

StudyandGrad

eConclusions

Result

sConclusion


at


ion

wakin

gimprovementinearlymorn

ing

cosleeping;33%repor

ted

71%ofparentsreportedfewernig

htsP=1.0)

(24.569.8vs32.2624.7mi

n;

wakingaftersleepons

et

45.6627.6;P=.039)butn

ot

latency(62.2633.33min

vs

Actigraphyshowedimproveds

leep

Sampl

e

TABLE

1Continued

(Tennesse

e)

ASDwithsleepconcer

ns

follow-

up1moafterend

consecutivewee

ks;

3to10ywithclinicaldiagnosis

of

Included:20familiesofchildrenaged·Three2-

hsessionsfor3

Reedetal,200

931

intervention

s

Behavioral/

educational

to6mg

after4wk,increasedos

e

Allchildren:ifnorespons

e

after2wk

increaseddoseto3m

gtimeIfnorespons

e,

30to60minbeforebe

dofbipolardisorde

r

Excluded:childrenwithadiagnosisAged$6y,1.5mgmelatoninSleep

diary

enuresis

)sleepinessand/

orincreased

hadadverseeffects(morni

ng

treatm

ent.Threechildr

en

reportedworsesleepaft

er

amajorconcern,and1

%3mg

13%sleepproblemsremai

ned

medications

)by1mgevery2wkupto

sleepdisorder(Tenness

ee)

stillhadconcerns;fo

rseverityofASD,use

of

noresponse,increas

ed

60%hadimprovedsleepb

ut

otherpsychiatricconditio

ns,

beforebed.After2wk,i

frecommendedtotakemelat

onin

diagnosedwithautism

previo

usly

problemsnolongeraconcer

n;

(includingsleephygie

ne,

melatonin30to60mi

n

Afterinitiation,25%withsle

ep

Chartreviewofclinicnot

es

Included:107childrenaged2to18yAged,6y,.75-

1mg

otheradverseeffec

ts

notescalate

d)

Loosestoolsin1child;n

o

actigraphy,thedosew

as

changeinlaborator

yfindings.

nightsperweekb

yChildsubscaleonthePSI.

No

within30minon$5

compulsive,andtheDi

fficult

d efinedasfallingaslee

p

Scale

RBSstereotypeda

nd

responseoccurre

d,

prolactin).HagueSideEff

ects

hyperactivity,andaffec

tive,

sleepeducationtraini

ng

response(ifasatisfact

ory

testosterone,FSH,LH,

and

withdrawn,attention-

deficit/

mgto6mgbasedon

addressed,andparentsrecei

ved

cortisol,estroge

n,

duration,CBCLsubscale

sof

medicalcomorbiditiesw

ere

escalatedfrom1mgto

3renalfunction,corticotro

pin,

sleep-

onsetdelayandsleep

periods.Dosewa

sBeforemelatonintreatm

ent,

pr

ofileincludingliverand

notedinCSHQsubscales

of

protocolbasedon3-

wk

takingpsychotropicmedicati

ons.

fi ndings(CBC,m

etabol

ic

improvementswereal

so

Excluded:childrenwithepileps

yor

Optionalescalatingd

ose

CBCL,RBS,PSI.Laborat

ory

Sign

ificantlysignificant

levelIII

Pre/post-

Nocontrol,

Andersenetal,200

830Pre/post-

control,LevelII

StudyandGrad

e

TABLE

1Continued

childrenwithautis

mdaytimesleepiness

indisorderedbreathing,

or

waking,parasomnias,sl

eep

wakings,earlymorni

ng

andsleepanxietybutnotn

ight

resistance,latency,durat

ion,

parentsimprovesbedti

me

Educationalintervention

with

sleepiness(P=.09

6)

(P=.625),anddayti

me

sleep-

disorderedbreathing

(P=.508),parasomnia(P=.60

7),

(P=.022)butnotnightwakin

gs

(P=.003),andsleepanxi

ety

latency(P=.004),durati

on

bedtimeresistance(P=.00

1),

improvedCSHQscoresf

or

Educationalinterventionsho

wed

CSH

Q

childrenwithAS

Dsleepproblemsi

ntreatm

enttoredu

ce

Melatoninisasafe,effecti

ve

Conclusions

Result

sConclusion


at


ion

Sampl

e


SUPPLEMENT ARTICLE


BEARS,B=Bedtimeproblems,E=ExcessiveDaytimeSleepiness,A=AwakeningsD

uringtheNight,R=RegularityandDurationofSle

ep,S=Snoring.

AdolescentSleepWakeSca

le40

BEAR

S17

BehavioralEvaluationofDisordersofSleepS

cale39

FamilyInventoryofSleepHabi

ts38

Adolescent

asleep,awakening,reinitiatingsleep,andwakef

ulness

Twenty-

eightitemsroleinto5subscales:goingtobed,falling

andsnorin

gwakecycles(bedtime,waketime)andaveragesleepd

uration;

children);awakeningsduringthenight;regularityof

sleep/

behaviorstypicallyassociatedwithdaytimesomno

lencein

fallingasleep);excessivedaytimesleepiness(i

ncludes

Fivesleepdomains:bedtimeproblems(di

fficultygoingtobedand

facilitators;andapnea/

bruxism

sensitivitytotheenvironment;disorientedawakenin

g;sleep

Fivetypesofsleepproblems:expressivesleepdisturb

ances;

routine,andsleepenvironm

ent

Twelveitems,includingdaytimeandprebedtimehabits

,bedtime

Assessessleepqualityinadolescentsaged11t

o21y

Parent

Assesses5sleepdomainsinchildrenaged5to

18y

Assessessleepbehaviorsinchildrenaged5to

12yaged3to10y

Autism

spec

ificquestionnaireassessingsleephygieneinchildren

Parent

Parent

Parent

disorderedbreathi

ng

maintenance,daytimesleepiness,sleeparousal,an

dsleep-

Twenty-

sixitemsthatroleinto6subscales:sleepinitiationand

SleepDisturbanceScaleforChildr

en37

Parent

5to15y

Characterizessleepdisordersoverthepast6moinchildr

enaged

developingchildr

en

autism

,developmentaldelaywithoutautism

,andt

ypically

AssessestheCSHQ(seeabove)inchildrenaged2to5.5y

with

Children(Goodlin-

Jonesetal,2008)23

Children’sSleepHabitsQ

uestionnaireinToddlersandPr

eschool

2000

)36

CSHQ(Owenset

al,

Questionnair

eRespondent

Form

at

Parent

SameastheCSHQ(abov

e)sleepines

sparasomnias,sleep-

disorderedbreathing,anddaytime

sleeponsetdelay,sleepduration,sleepanxiety,night

wakings,

Forty-

fi veitemsthatrollinto8subscales:bedtimeresistance,

medicaldimensionsinchildrenaged4to

10y

Assessessleepbehaviorsacrossarangeofbehavior

aland

Description

TABLE

2SleepQuestionnaireOptions

stimulatinghorm

one;LH,luteinizinghorm

one;MCV,m

eancorpuscularvolume;PSI,ParentalStressIndex;RBS,RepetitiveBehaviorScale;SI,SensoryIntegration;SS,SpectrumSupport;TTM,

ThaiTraditionalMassage.

CARS,ChildhoodAutism

RatingScale;CBC,completebloodcellcount;CBCL,ChildBehaviorChecklist;CGI,ClinicalGlobalIm

pression;CI,co

nfidenceinterval;CR,controlledrelease;FISH,FamilyInventoryofSleepHabits;FR,fastrelease;FSH,follicle-

Excluded:notspec

ified

day-

timebehavior)

providedstatisticsf

or

numbersnotprovided;o

nly

gettingoutofbed(actu

al

bed)

readingbeforebedti

me

self-

stimulatingbehavior,and

numberoftimeschildleftt

he

therapist)or15mino

f

fussing/

restlessness,crying,

stimulatingbehavior,

and

parents(trainedb

ywithautism

(Florid

a)

therapygroupwithregard

torestlessness,crying,s

elf-

massagetherapy

by

recruitedfromschoolforchild

ren

Greaterdeclinesforthemass

age

Sleepdiaries(fussin

g,

For1mo,received15-

min


6y

Excluded:nonespec

ified

df=16,160;P,.89)

aromatherapy(F=0.

59;

wasnotaffectedb

ydf=16;P=.21).Sleepdurati

on aromatherapy(

x2=20.19;

beforebe

d offootandleg∼2hour

sdifferwithandwitho

ut

P=.30).Nightwakingsdidn

ot

oil)over24dviamassa

ge

withautism

(UnitedKingdo

m)

onsettime(F=1.27;df=4.15,4

1.5;

onset,duration,wakin

gs)

lavenderoilingrapese

ed

aresidentialschoolforchildr

en

diagnosedwithASDfro

m statisticallysign

ificantsleep-

30-

minintervalrounds(sleep

aromatherapy(2

%

SleepdiaryrecordedbystaffonParticipantsdidnotdemons

trate

Included:12childrenaged12to15yThreeadministrati

onsof

treatm

ent(13massag

es)

thoseunabletocomplete80

%of

for8wk

contraindicationsforTTMa

nd

Excluded:thosewi

thTwo60-

minTTMandSI

RCT,levelI

V

Escalonaetal,200

135CaseserieslevelI

I

Williams,200

634RCT,levelI

I

(Thailand

)wereexperimental(SI+TT

M)

8wk

putintocontrolgroup(SI)and

30

Two60-

minTTMandSIfor

diagnosedwithautism

;30w

ere

Sleepdiar

yIncluded:60childrenaged3to10yTwo60-

minstandardSIor

Piravejetal,200

933

alternativemedici

ne

Complementarya

nd

StudyandGrad

e

TABLE

1Continued

withASDmorethanreadi

ng

gettingoutofbedinchildre

nself-

stimulatingbehavior,and

fussing/

restlessness,crying,

Massagebeforebeddecrea

seswaking

sonset,duration,andnig

ht

treatm

enttoaffectsle

ep

Aromatherapyisnotaneffec

tivestandardS

Inotm

orethancomparedw

ith

sleepinchildrenwithASD

but

TT,beforebedtimeimpro

ves

6.3respectively;P=.8

5)

statisticallysign

ificant(5.7vs

andmassagegroupsw

eren

ot

behaviorscoresofthecontr

ol

betweenpre-andpost-

sleep

vs8.2;P,.001).Thedifferenc

eimprovedsleepbehavior(1

3.9

5.3;P,.001).StandardS

I

Massageimprovedsleepscores(11

.5vs

Conclusions

Result

sConclusion


at


ion

Sampl

e


SUPPLEMENT ARTICLE

insomnia in children (not specific toASD) were identified.The results of the systematic literaturereview demonstrate that treatmenttrials are limited in the ASD population.There are 3 categories of treatment:pharmacologic/biologic treatments,behavioral/educational

interventions,and complementary and alternativemedicine.

The evidence base to date shows

limitedevidence for the use of medications totreat insomnia in children who haveASD. The most evidence exists for theuse of supplemental melatonin, anindoleamine with sleep-promoting andchronobiotic (sleep phase shifting)properties considered a nutritional

supplement by the US Food and DrugAdministration. Several small,

ran-domized controlled trials (RCTs) dem-onstrated the efficacy of supplementalmelatonin in treating insomnia inchildren who have ASD,27–29 althoughlarger studies are needed. Melatoninseems to be relatively safe based o

nthese trials and on other series.30Other pharmacologic interventionssuch as risperidone, secretin, L-carni-tine, niaprazine, mirtazapine, and

clo-nidine, as well as multivitamins andiron, have limited evidence supportingtheir use in treating insomnia in ASD.The research evidence to date does notsupport the efficacy of other supple-ments or vitamins.

Behavioral interventions are clearlybeneficial for typically developing chil-dren experiencing significant insom-nia.21 However, few treatment

trialsfound that behavioral treatments pro-vide consistent success rates in chil-dren who have ASD, particularly thoseexperiencing sleep-onset insomnia. Thesystematic review of the literature ide

n-tified 2 studies examining the

efficacyof behavioral treatment of

insomniain children who have ASD.31,32 Each

ofthese studies demonstrated statisti-cally significant improvements in sleep


posttreatment. Both studies used mul-ticomponent treatments, although theyvaried with respect to the specificcomponents of treatment. However,they were representative of treatmentscommonly used in clinical practice as

well as supported as effective in thegeneralpediatric

population.studies used extinction and positivereinforcement as

treatments.Both

studies provided parent training, asfollows: (1) identifying a treatmentgoal/treatment target for therapy; (2)discussion of how the sleep

problem ismaintained by conditioning/learning;and (3) emphasis on establishing a de-velopmentally

appropriatebedtime

and a consistent bedtime routine. Othertreatment components addressed in a

single study included sleep hygiene in-structions, use of effective instructions/directions to shape appropriate sleepbehavior, and use of the bedtime passprotocol.23 The studies did not addressrelative efficacy of these individual treat-ment components.Complementary and alternative medi-cine therapies addressed in the litera-ture review include massage therapyand aromatherapy.33–35 The systematicreview found no evidence to supportthese therapies for insomnia in chil-dren who have ASD. Neither of thegraded studies examining the efficacyof massage therapy or aromatherapyfor insomnia in children who have ASDled to statistically significant improve-ments in sleep posttreatment.33–35

Results of the GuidelineDevelopment

Based on the feasibility testing, a

numberof observations resulted in the devel-opment of resources to assist cliniciansin the application of the practice pathway.After reviewing the literature and con-ducting pilot testing, the ATN SleepCommittee developed and refined theinsomnia practice pathway and made the

following consensus recommendations:

A. General pediatricians, family careproviders, and autism medical spe-cialists should screen all childrenwho have ASD for insomnia.

This screening is best done by askinga short series of questions targetinginsomnia, such as those from theCSHQ, and asking if the parent consid-ers these a problem. These questions

TABLE 3 Questionnaire to Help Identify Underlying Medical Conditions are: (1) child falls asleep within 20minutes after going to bed; (2) childfalls asleep in parent’s or sibling’s bed;(3) child sleeps too little; and (4) childawakens once during the night. Thesequestions were selected on the basisof review of the CSHQ and expert con-sensus. The ATN database was alsoreviewed (n = 4887), and we foundthat 81% of parents who reportedthat their child awakening more thanonce during the night was a problemalso answered affirmatively to thequestion “Does your child awaken onceduring the night?” Therefore, to limitthe questions asked, we did not in-clude “Does your child awaken morethan once during the night?” Askingspecific questions is essential becauseparents may not volunteer concernsabout insomnia given their concernswith behavioral issues (although theseissues may be secondary to the in-somnia). Identifying significant insom-nia is paramount given its impact ondaytime functioning, not only for thechild with ASD but also the family. Table2 lists available questionnaires.

B. The evaluation of insomnia shouldinclude attention to medical


SUPPLEMENT ARTICLE

contributors that can affect sle

ep(including neurologic conditions an

dother sleep disorders that contr

ib-ute to insomnia).

These contributors should be

ad-dressed because their treatment mayimprove insomnia. Within the ATN, wehave developed a list of questions formedical contributors, including gas-trointestinal disorders, epilepsy, pain,nutritional issues, and other under-lying sleep disorders responsible forinsomnia, including sleep-disoderedbreathing and restless legs symptoms(Table 3) that pediatricians can in-corporate within their review of sys-tems. Psychiatric conditions, such asanxiety, depression, and bipolar disor-der, should be considered becausethese may contribute to insomnia. Fi-nally, because many medications con-tribute to insomnia, a careful review ofmedications should be performed.

C. Educational/behavioral

interventions

are the first line of treatment, after

excluding medical contributors. How-ever, if an educational (behavio

ral)approach does not seem feasibl

e,or the intensity of symptoms h

as

reached a crisis point, the use of phar-macologic treatment i

s considered.

Educational/behavioral

approaches tothe treatment of insomnia are advo-cated as a first-line treatment in typi-cally developing children.21 In childrenwho have ASD, educational/behavioralapproaches are also recommended,especially because these children maynot be capable of expressing adverseeffects caused by the medications. Thecore behavioral deficits associatedwith ASD may impede the establish-ment of sound bedtime behaviors androutines. These include: (1) difficultywith emotional regulation (eg, ability tocalm self); (2) difficulty transitioningfrom preferred or stimulating activi-ties to sleep; and (3) deficits in com-munication skills affecting a child’sunderstanding of the expectations of

parents related to going to bed and fall-ing asleep. Conversely, given preferencesfor sameness and routine, children whohave ASD may adapt well to establish-ment of bedtime routines, especially ifvisual schedules are implemented.

The ATN has developed an educationaltoolkit for parents that consists ofpamphlets to promote good sleephabits; a survey to assess for habitsthat may interfere with sleep; samplebedtime routines, including a visualsupports library, tip sheets for imple-menting the bedtime routine, andmanaging night wakings; and a sleepdiary. The toolkit is being tested forfeasibility in an ongoing research pro-ject funded by the Health Resourcesand Services Administration of parentsleep education at 4 ATN sites and isalso being used in clinical practicethroughout the network. As with othereducational/behavioral approaches,the success of this toolkit depends onappropriate implementation by par-ents, with the guidance provided bypractitioners an essential element formany families. Families can often beencouraged to implement educational/behavioral strategies when presentedwith these tools, especially if they re-ceive hands-on instruction in the toolsand are provided with an explanation ofwhy a behavioral approach is recom-mended. However, some families maybe in a state of crisis or may not bewilling or able to use the behavioraltools. These families may be challengedby difficult daytime behaviors in theirchild or by financial concerns. Thesechildren might require pharmacologictreatment. In addition, practitioners maynot be able to provide sufficient in-struction in the tools for a family to besuccessful with their implementation.Therefore, there is the option in thepractice pathway (Fig 2, Box 5b) ofmedication or consultation to a sleepspecialist if the family is unwilling orunable to use an educational approach,

depending on the comfort level of thepediatrician.

Behavioral Treatments for Insomnia

The behavioral treatments most com-monly used to treat insomnia in chil-dren who have ASD include behavioralmodification strategies such as extinc-tion (eg, withdrawal of reinforcementfor inappropriate bedtime behaviors)and positive reinforcement of adaptivesleep behavior. Sleep hygiene instruc-tions (eg, appropriate sleep schedulesand routines) often accompany behav-ioral modification protocols. Behavioralinterventions are effective in the treat-ment of insomnia in typically developingchildren.21 However, the evidence base

for effectiveness of such interventions inchildren who have ASD is limited. Thedata from the literature review providepreliminary support for the use of be-havioral modification to treat insomniain children who have ASD. These datawere the basis for the development of aneducational toolkit used to guide behav-ioral management of insomnia in theinsomnia practice pathway.

Alternative Treatments for Insomnia

The most common alternative therapywith a presence in the literature is mas-sage therapy.33,35 However, the results donot demonstrate consistent, statisticallysignificant improvements in sleep.

Pharmacologic Treatments forInsomnia

Although medications and supplementsare often used to treat insomnia experi-enced by children and adolescents whohave ASD, the evidence base for phar-macologic treatment is limited. At thistime, there are no medications approvedby the US Food and Drug Administrationfor pediatric insomnia. The most evi-dence exists for the use of melatonin.

D. Clinicians should assure timelyfollow-up to monitor progress andresolution of insomnia.


Assuring adequate follow-up is crucialwhen treating children who have ASDand significant insomnia. Follow-upshould occur within 2 weeks to 1month after beginning treatment. Theprovider and family should expect tosee some benefits and improvementswithin 4 weeks. Follow-up may be con-ducted by telephone or in person.Timely follow-up allows for fine-tuningof treatment interventions, support ofparents, and provision of referrals ifneeded.In addition to short-termfollow-up (eg, 1–2 months), at long-term follow-up (eg, 1-year visit) thesteps from the beginning of the prac-

tice pathway should be repeated.

As outlined in the practice

pathway,treatment of insomnia can be initiatedby the general pediatrician, primarycare provider, or autism medical spe-cialist. Many children will improve withthese initial interventions. Consultationwith a sleep specialist is indicated ifinsomnia is not improving with theseinitial interventions or when the in-somnia is particularly severe, causingsignificant daytime

impairmentplacing the child at risk for harm whileawake during the night. For thosechildren who have ASD and are takingmultiple medications for sleep wheninitially assessed by the health careprovider, consultation wit

h a sleepspecialist may be indicated, dependingon the comfort level of the provider.Other indications for consultation witha pediatric sleep specialist may includewhen underlying sleep disorders areresponsible for the

sleeplessnesssymptoms (including

sleep apnea,restless legs syndrome, periodic limbmovements of sleep, and unusual night-time behaviors [parasomnias] such assleepwalking or sleep terrors).

Results of the Field Testing

Results of the pilot phase indicat

edchallenges in implementing the practicepathway due to a number of conflicts,

including: (1)competingdemands on thepediatric provider in a busy clinicalpractice; (2) knowledge level of the pe-diatric provider; and (3) when consul-tation to the sleep specialist occurs,ensuring communication back to thepediatric provider.

In response to these barriers, we de-veloped the following resources: (1)a short set of screening questions forinsomnia as well as a checklist formedical conditions contributing to in-somnia (Table 3); and (2) a sleep edu-cation toolkit, available in hard copy aswell as on the internal ATN Web site(www.autismspeaks.org/atn) that willfacilitate parent teaching.

Additional issues were identified re-lated to provider comfort level in thefollowing areas: (1) assessing formedical or sleep contributors them-selves rather than referring to a spe-cialist, which led us to modify thepractice pathway to allow for bothoptions; (2) providing education tofamilies in use of the toolkit, which af-fected the length at which follow-upoccurred (eg, a second visit witha nurse educator might be needed fortoolkit implementation if the providerwas too busy to educate families at thetime of the initial clinic visit); and (3)treating insomnia with medications ontheir own versus referring to a sleepspecialist. When a child was referred tothe sleep specialist, ensuring that thesleep specialist communicated backto the provider regarding recommen-dations was also an issue related toapplying the practice pathway in ourfield testing, particularly as related tofollow-up care.

We modified the flow of the practicepathway in response to feedback dur-ing the field testing. Initially, the prac-tice pathway prioritized evaluationand treatment of medical contributorsbefore implementing educationalmeasures, such as the toolkit. However,based on the feedback of clinicians, the

evaluation/treatment of medical con-tributors and the implementation ofeducational measures became a paral-lel process as opposed to a sequential

“first–then” approach.

DISCUSSION

We report here on the development o

fa practice pathway for the evaluationand management of insomnia in chil-dren who have ASD. There are severalkey points of this practice pathway.First, general pediatricians, primarycare providers, and autism medicalspecialists should screen all childrenwho have ASD for insomnia becauseparents may not volunteer sleep con-cerns despite these concerns beingcontributors to medical comorbiditiesand behavioral issues. Second, theevaluation of insomnia should in-clude attention to medical contributorsthat can affect sleep, including othermedical problems that encompassgastrointestinal disorders, epilepsy,psychiatric comorbidities, medications,and sleep disorders including sleep-disordered breathing, restless legssyndrome (unpleasant sensations in

thelegs associated with an urge to move),periodic limb movements of sleep(rhythmic leg kicks during sleep), andparasomnias (undesirable move-ments or behaviors during sleep,such as sleepwalking, sleep terrors, orconfusional arousals). In parallel withthis screening, the need for therapeu-tic intervention should be determined.We also determined that educational/behavioral interventions are the firstline of treatment, after excludingmedical contributors. If an educa-tional (behavioral) approach does notseem feasible, or the intensity ofsymptoms has reached a crisis point,the use of pharmacologic treat-ment is considered. Finally, cliniciansshould assure timely follow-up tomonitor progress and resolution ofinsomnia.


http://www.autismspeaks.org/atn

SUPPLEMENT ARTICLE

This practice pathway expands the l

it-erature that currently exists for typi-cally developing children related toscreening and management.5,7–9 Therationale for developing a practicepathway that uniquely addresses thispopulation is because children whohave ASD, and their families, haveunique needs. For example, medical,neurologic, and psychiatric comorbid-ities are common in children who haveASD, as is the use of medications thatinfluence sleep. In addition, parents ofchildren who have ASD, struggling withthe stressors related to their child’sdisability and the often accompanyingbehavioral challenges, may not volun-teer sleep to be of concern. In turn,pediatric providers may not ask aboutsleep due to competing medical andbehavioral issues. Furthermore, sleepproblems are more common in chil-dren who have ASD than in childrenof typical development,2,3 and theirtreatment may impact favorably ondaytime behavior and family function-ing. Given these factors, we do recog-nize that children who have other

disorders of neurodevelopment couldalso benefit from this practice pathway,as they share common features withchildrenwho have ASD,

including

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A Practice Pathway for the Identification, Evaluation, and Management ofInsomnia in Children and Adolescents With Autism Spectrum Disorders

Beth A. Malow, Kelly Byars, Kyle Johnson, Shelly Weiss, Pilar Bernal, Suzanne E.Goldman, Rebecca Panzer, Daniel L. Coury and Dan G. Glaze

Pediatrics 2012;130;S106DOI: 10.1542/peds.2012-0900I

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