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Sleep Medicine 10 (2009) 446–456

Original Article

Subjective and objective measures of sleep in childrenwith attention-deficit/hyperactivity disorder

Judith Owens a,*, R. Bart Sangal b, Virginia K. Sutton c,1, Rosalie Bakken d,Albert J. Allen d, Douglas Kelsey d

a Brown Medical School, Ambulatory Pediatrics, Potter 200, 593 Eddy Street, Providence, RI 02903, United Statesb Clinical Neurophysiology Services PC, Troy, MI, United States

c i3 Research, Cary, NC, United Statesd Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, IN, United States

Received 30 October 2007; received in revised form 11 March 2008; accepted 15 March 2008Available online 6 August 2008

Abstract

Objective: To compare objective and subjective measures of sleep in children with attention-deficit/hyperactivity disorder (ADHD)and healthy control subjects.Methods: Included were 107 unmedicated children with ADHD and 46 healthy control subjects, all aged 6–14. Sleep–wake patternswere monitored with actigraphy for at least five consecutive days. Subjects and parents completed daily electronic diaries assessingsleep and daytime behavior.Results: Actigraphy data from 80 ADHD patients and 45 control subjects showed that, compared to the healthy control group, theADHD group experienced shorter actual sleep time (defined as time in minutes [from sleep onset to final morning awakening] of allepochs scored as sleep [i.e., excluding total duration of all epochs scored as ‘‘wake”]) (489.39 vs. 460.30 min, p = .001), significantlyfewer sleep interruptions (44.45 vs. 35.33, p < .001), but more total interrupted sleep time (44.49 vs. 56.70 min, p = .002). Child dia-ries indicated children with ADHD had significantly more daytime sleepiness and difficulty getting up and less refreshing sleep. Par-ent diaries indicated children with ADHD had significantly more behavioral difficulties than the control group.Conclusions: Results suggest children with ADHD have reduced sleep quantity and more disturbed sleep on actigraphic measures,reduced sleep quality on the self report, and more problematic behaviors on the parent report. Clinical interventions for childrenwith ADHD who present with sleep problems should include screening for etiologic and exacerbating factors, institution of behav-ioral-management strategies, and consideration of pharmacologic treatment targeted toward evening ADHD symptoms.� 2008 Elsevier B.V. All rights reserved.

Keywords: Children; ADHD; Actigraphy; Behavior; Sleep patterns; Sleep problems

1. Introduction

Attention-deficit/hyperactivity disorder (ADHD) isthe most common pediatric psychiatric disorder, esti-

1389-9457/$ - see front matter � 2008 Elsevier B.V. All rights reserved.

doi:10.1016/j.sleep.2008.03.013

* Corresponding author. Tel.: +1 401 444 4239; fax: +1 401 4446218.

E-mail addresses: owensleep@gmail.com, mellingersl@lilly.com (J.Owens).

1 Dr. Sutton was a full-time employee of Eli Lilly and Company,Indianapolis, IN, when study was conducted and manuscript drafted.

mated to occur in 3% to 7% of school-age children [1].Core symptoms include a functionally significant levelof inattentiveness and distractibility (difficulty stayingon task, completing work) and also frequently involveimpairments in executive functioning (organization,working memory), as well as increased behavioral andverbal impulsivity (talking out of turn, interrupting)and motoric restlessness (difficulty remaining seated,fidgeting). Sleep problems, particularly difficulty initiat-ing and maintaining sleep, also are frequently reported

J. Owens et al. / Sleep Medicine 10 (2009) 446–456 447

in children and adolescents with ADHD in clinical prac-tice. In fact, the 3rd Edition of the Diagnostic and Statis-

tical Manual of Mental Disorders [2] listed restless sleepas a diagnostic criterion for ADHD, although this crite-rion was eliminated from subsequent DSM editions.Despite this connection, studies attempting to examinedifferences in sleep between children with ADHD andcontrols do not consistently support this clinical experi-ence, nor do they always concur in their findings.

Specifically, most of the ‘‘objective” studies of sleeputilizing overnight polysomnography (PSG) or actigra-phy, including two recent systematic reviews of the liter-ature [3,4], have failed to find consistent differences insleep architecture and patterns between children withand without ADHD [5–9], with the possible exceptionsof increased nocturnal movements [5,7,9] and greaternight-to-night variability in sleep patterns among chil-dren with ADHD [8,10,11]. Results of objective studiesmeasuring daytime sleepiness, however, do seem to con-sistently suggest that children with ADHD fall asleepfaster during the day compared to control children[12,13]. These studies used the multiple sleep latency test(MSLT), a series of five scheduled 20-min daytimeopportunities to nap, to measure physiological tendencyto fall asleep. Despite having overnight PSG sleepparameters comparable to those of controls, childrenwith ADHD were more likely to fall asleep, to have ashorter average sleep onset latency, and to show exces-sive physiological tendencies to fall asleep, suggestingthat at least some of these children may actually behypo-aroused compared to children without ADHD.Additional support for the existence of a hypo-arousedstate in these children comes from the results of a recentstudy [14] that found children with ADHD had lowerrates of electroencephalogram (EEG) cyclic alternatingpatterns (CAP) on nocturnal polysomnography, an indi-cator of possible sustained arousal instability.

In contrast to the relative lack of consistent differ-ences in objectively measured nocturnal sleep parame-ters, subjective parent reports almost universallyindicate a high frequency of significant sleep problemsin children with ADHD. These include bedtime resis-tance [15,16], delayed sleep onset [17,18], frequentnight waking [18–20], frequent motor movements dur-ing sleep [5,21], and morning/daytime fatigue[18,22,23], with prevalence rates and levels of intensitygenerally two or three times greater than those of con-trol-group children. More recent studies suggest thatmany of these sleep disturbances may be attributedto either medication-related effects or to commoncomorbid psychiatric conditions (such as opposi-tional-defiant disorder [ODD] and anxiety disorders),rather than ADHD [24,25]. Furthermore, the correla-tion between objective sleep measures and parent orself reports in the few studies that have examined thisissue has been poor [26,27].

Importantly, many of the objective and subjectivestudies of sleep in children with ADHD have methodo-logical shortcomings, such as small sample sizes andselection bias, variability in ADHD diagnostic criteria,inadequate assessment for comorbid psychiatric condi-tions, variations in concomitant medication status, andvariability in the nature of control groups. Furthermore,few studies have attempted to assess or exclude subjectswith ‘‘organic” sleep disorders, such as obstructive sleepapnea (OSA) and periodic limb movement disorder(PLMD). The latter point is particularly important inlight of empirical evidence suggesting deficits in atten-tion, memory, executive functioning, externalizingbehaviors (e.g., impulsivity, hyperactivity, aggression),and mood disturbance among children with organicsleep disorders and those with ADHD [28–31].

In an attempt to elucidate the origin of these contra-dictory findings, a few published studies also have com-pared sleep variables across ADHD subtypes andseverity levels. These studies again have failed to findconsistent between-group differences. For example, sev-eral studies have suggested that those children withADHD predominantly characterized by increasedhyperactivity are at greater risk of experiencing impair-ments related to sleep [18,23,32], whereas others havefound no significant differences related to ADHD sub-type or severity [27].

The goal of this study was to further elucidate therelationship between ADHD and sleep quality by com-paring sleep in a large sample of children with ADHD tothat of control-group children using simultaneous objec-tive (actigraphy) and subjective (parent and child elec-tronic daily diaries) measures. This study incorporatedseveral important methodological improvements toeliminate some of the confounding variables that havelimited interpretation of previous studies. First, allADHD diagnoses were confirmed using strict criteriaprovided in the 4th Edition of the Diagnostic and Statis-tical Manual of Mental Disorders (DSM-IV) [33], anddata from the ADHD patient group were analyzed interms of both ADHD subtype and severity. In addition,potential subjects with comorbid psychiatric disorders(with the exception of oppositional-defiant disorder),were excluded from participation, and no ADHD sub-jects had taken psychotropic medication for at leastseven days prior to assessment of sleep. Subjects takingprescription or over-the-counter, central nervous sys-tem-active medicines (including caffeine) on a daily basiswere also excluded. All subjects were screened andexcluded for symptoms suggestive of OSA and restlessleg syndrome (RLS)/PLMD, and a subset of the ADHDsubjects were polysomnographically screened to docu-ment the presence or absence of a primary sleep disor-der. The study also used a control group of healthysubjects who had been evaluated and excluded for psy-chiatric disorders, including ADHD. The child and par-

448 J. Owens et al. / Sleep Medicine 10 (2009) 446–456

ent sleep and behavior diaries utilized electronic datacapture technology to improve the quality and reliabilityof the data, as well as compliance. Finally, this studycollected actigraphy data for at least five consecutivedays (range: 5–12 days) and included both weekdayand weekend sleep patterns in order to better assessnight-to-night variability in sleep patterns.

2. Methods

2.1. Subjects

Subjects were males and females, aged 6–14 years,from two United States study centers, and included107 children with ADHD and 46 healthy children with-out ADHD. There were no significant differences inrecruitment procedures at the two study sites. All sub-jects were compensated for time and travel in accor-dance with IRB standards, and compensation was thesame at both sites. Controls were recruited from thecommunity through local newspaper advertising and fly-ers. All participants were administered the Attention-Deficit/Hyperactivity Disorder Rating Scale-IV-ParentVersion: Investigator Administered and Scored(ADHDRS-IV-PI), an 18-item scale with each item cor-responding to one of the 18 symptoms contained in theDSM-IV [33] diagnosis of ADHD. Each item is scoredon a 0 to 3 scale (0 = never or rarely; 1 = sometimes;2 = often; 3 = very often) [34]. The rating scale assessessymptom severity over the past week as scored by aresearcher interviewing a parent. Both a total scoreand subscores for inattention and hyperactivity/impul-sivity were computed.

Participants with ADHD had to have ADHDRS-IV-PI scores at least 1.0 standard deviation (SD) above ageand gender norms for their ADHD subtype (predomi-nantly inattentive, hyperactive/impulsive, or combined)at Visits 1 and 3, and they had to be diagnosed withADHD using the DSM-IV [33] criteria. ADHD diagno-ses were made using clinical evaluation and administra-tion of several modules of the Kiddie Schedule forAffective Disorders and Schizophrenia for School-AgedChildren-Present and Lifetime version (K-SADS-PL)[35]. Scores P4 (moderate) on the Clinical GlobalImpression-Severity of Illness (CGI-S) seven-point scalewere also required.

Control subjects were judged to be medically healthy,had ADHDRS-IV-PI scores <1.0 SD above age andgender norms at Visit 1, and had no current or past psy-chiatric illness (including ADHD) as assessed on the K-SADS-PL. Additional inclusion criteria for both groupswere a full-scale Wechsler Intelligence Scale for Children(WISC) score of P80 and agreement by the subject notto use caffeinated beverages during the study.

Exclusion criteria for both groups included treatmentwith any investigational drug within 30 days of study

entry; a history of bipolar disorder or psychosis or useof antipsychotic medicines within four weeks of studyentry; an affective or anxiety disorder diagnosis asassessed by the K-SADS-PL; serious suicidal or homi-cidal risk; current or past substance abuse; and use ofany prescription, over-the-counter central nervous sys-tem-active or sedating medicines. Both ADHD and con-trol subjects were excluded if they had a history orcurrent symptoms suggestive of a primary sleep disor-der, such as OSA or RLS. Subjects were considered tohave the primary sleep disorder RLS if they reportedlower extremity discomfort exacerbated by inactivity atbedtime, and OSA if the parent reported loud and fre-quent snoring, snoring with observed apneic episodes,or snoring with excessive daytime sleepiness (EDS).Only one subject was excluded from the protocol atthe screening visit because of a history of snoring withEDS; no patients were excluded due to symptoms ofRLS. Subjects with sleep initiation or maintenanceproblems not attributable to OSA or RLS were notexcluded.

Subjects meeting diagnostic criteria for ODD werenot excluded because of the high level of comorbidityof ODD in most ADHD populations, occurring in30% to 60% of children with ADHD [36–38]. It shouldbe noted that further statistical analyses (post hoc anal-yses) were conducted to assess the effect of comorbidODD on sleep parameters.

Approximately half the entered ADHD subjects(n = 40) also volunteered for two consecutive (one accli-matization and one recording night) overnight PSGstudies conducted 10–24 days after the screening visit.Details of the PSG monitoring and criteria for OSAand PLMD are described elsewhere [39]. Writteninformed consent (and patient assent when age-appro-priate) was obtained from each participant’s parent orlegal guardian prior to study entry. The study wasapproved by each site’s institutional review board andwas conducted in accordance with the ethical principlesoriginating in the Declaration of Helsinki and consistentwith good clinical practices and applicable laws andregulations.

2.2. Actigraphy

Actigraphy uses a small, computerized deviceattached to the wrist to measure body movements.Movement patterns are analyzed and used to differenti-ate between sleep and wake time, thus providing estima-tions of sleep onset latency, total duration of sleep,number of arousals, and other variables. The reliabilityand validity of actigraphy has been established, andactigraphy data in children have been shown to correlatewell with data obtained using PSG on variables relatedto sleep [40]. Compared to PSG, actigraphy also hasthe advantage of measuring sleep patterns over a period

J. Owens et al. / Sleep Medicine 10 (2009) 446–456 449

of time (several days to weeks) in a more naturalistic(home) setting. The Actiwatch AW 64, from Mini MitterCompany, Inc., Bend, OR, was used in this study.

2.3. Study design

This study reports results from a set of baseline mea-sures collected during the initial study period of a longerdouble-blind crossover trial (results of which arereported separately [41]) comparing the effects of twicedaily atomoxetine and thrice daily methylphenidate onADHD treatment response and sleep parameters in chil-dren with ADHD. A secondary objective of the studywas to compare sleep in children with ADHD at base-line with that of healthy control children. The study per-iod comprised three visits over a range of 10–24 days.On Visit 1, the study was explained, and informed con-sent and medical histories were obtained. Physical andpsychiatric examinations, primary sleep disorder screen-ings, and ADHDRS-IV-PI and other scale administra-tion also occurred. All data were collected betweenJuly 2001 and August 2002.

2.4. Electronic diaries

Daily child and parent diaries were used to collectand transmit subjective data regarding both sleep anddaytime behaviors. Data were captured in the morningand evening each day using electronic individual hand-held personal digital assistants (PDAs; PHT EsendantLogPad) that automatically time-stamped the data andprovided built-in prompts and logic checks. The childdaily electronic diary included visual analogue scalequestions rating self-reported ease of getting up andsleepiness during the day (from ‘‘very easy” or ‘‘notsleepy at all” to ‘‘very hard” and ‘‘very sleepy”), timeto sleep onset the previous night (from ‘‘fell asleep rightaway” to ‘‘took more than 30 min to fall asleep”) andhow well the child reported sleeping the previous night(from ‘‘very badly” to ‘‘very well”).

Parent daily electronic diaries were also completedeach morning and evening and included similar ques-tions assessing difficulty getting out of bed; getting readyfor the day; how much inattention, arguing, or irritabil-ity the child exhibited that morning (on a scale of 0 to 4to indicate ‘‘not at all” to ‘‘extreme difficulty”); and thechild’s difficulties in the evening with doing homework,sitting still at dinner, playing quietly, being inattentive,arguing or struggling, losing his or her temper, transi-tioning activities, settling down, and falling asleep,respectively (from ‘‘none” or ‘‘not at all” [scored as 0],to ‘‘extremely” [scored as 4]).

Beginning on the evening of Visit 1 and continuing toVisit 3, subjects wore actigraphy monitors on their non-dominant wrists, and subjects and parents recorded datain actigraphy sleep logs. Visits 1, 2, and 3 occurred 5–12

days apart. Sleep logs and actigraphy data werereviewed with the parents at Visits 2 and 3 in order toresolve any discrepancies in the sleep data. All subjectswere asked to choose and maintain a ‘‘lights-out” orbedtime that was as close as possible to their habitualbedtime, and to deviate no more than 30 min beforeor after this stated bedtime on school nights (60 minon non-school nights) during the study period. Subjectswere asked to maintain their usual weekday/weekendmorning wake time schedule.

2.5. Actigraphy variables

For the purposes of this study, the primary actigra-phy variables measured were the following: sleep onset

latency (time in minutes from getting into bed/‘‘lightsout” to actigraphically defined sleep onset); actual sleep

time (time in minutes from sleep onset to final morningawakening of all epochs scored as sleep, i.e., excludingtotal duration of all epochs scored as ‘‘wake”; number

of sleep interruptions (number of time periods scoredas ‘‘wake” from sleep onset to final morning awakening;these periods could range in duration from one minute[one epoch] to over an hour, as long as the wake epochswere contiguous); and interrupted sleep time (the sum inminutes of the total number of one-minute epochsscored as ‘‘wake” from sleep onset to final morningawakening). Two additional actigraphic variables werecalculated from those just described: total sleep interval

(total time in minutes from sleep onset to final morningawakening, which was computed as the sum of actualsleep time and interrupted sleep time), and sleep effi-

ciency (actual sleep time divided by total time in bed).Because many subjects did not reliably press the actigra-phy button to indicate morning wake times (‘‘sleepend”), wake-up time was instead computed as the sumof bedtime, sleep onset latency, and total sleep interval.Bedtime refers to the time that each child actually wentto bed each night, and was recorded by pressing a but-ton on the actigraph watches. It should be noted thata ‘‘medium” threshold setting (40) for detecting wakeperiods was used for both the ADHD and controlgroups. Although this may have resulted in some degreeof over-estimation of wake time during the sleep intervalin the potentially more active ADHD group, it allowedfor direct comparison to the control group.

2.6. Data analysis

A sample size of 40 healthy control subjects and 60ADHD patients was determined sufficient to provide80% power to detect actigraphy differences betweengroups with an effect size of 0.55 or greater. Categoricaldemographic variables were compared across ADHDand healthy control groups using Fisher’s exact test.Group differences in continuous demographic variables

450 J. Owens et al. / Sleep Medicine 10 (2009) 446–456

were tested using analysis of variance (ANOVA) with aterm for group. Post hoc demographic variables werecompared for patients who elected to participate in pol-ysomnography and those who did not, using the samemethods. Differences between ADHD and healthy con-trol groups were analyzed for each actigraphy variableusing an ANOVA model with terms for group (ADHDor subject) and investigator. Within group changes weretested as being different from zero change using Stu-dent’s t-test. Post hoc differences were also comparedwithin ADHD subgroups by severity (mild/moderateversus severe), comorbid ODD (present or absent),and ADHD subtype (inattentive versus combined) usingan ANOVA model with terms for the subgroup of inter-est (e.g., mild/moderate or severe) and investigator.

For actigraphy, it was a priori specified that all sub-jects with at least 70% non-missing data at one visitinterval were to be included. Visit-level averages werecalculated if the criteria were met. The last visit intervalwas used if both visit intervals had sufficient non-miss-ing data.

Post hoc, two methods were used to assess variabilityin sleep onset latency and actual sleep time. First,Brown–Forsythe’s test was used to assess differences ingroup standard deviations (SDs) for these measures.However, since these SDs were based on averaging atthe visit over individual patient scores, a second testwas employed. Individual patient SD scores were com-puted across all available scores during visits when theywere compliant with the actiwatch. A log transforma-tion was applied to the SD scores, and ANOVA, withterms for group and investigator, was used to test forgroup differences in mean SD scores.

For child and parent electronic diaries, patients withat least nine records during the 14 day period followingstudy entry were included. Their averages during thistwo-week window were tested for group differencesusing an ANOVA model with terms for group andinvestigator. These criteria were similar to the a priori

specifications for the double-blind portion of the trial.Post hoc, Pearson’s correlation coefficient was com-

puted to test for linear associations among the actigra-phy and diary measures for all patients and alsowithin the ADHD patient group by subtype and severityof ADHD. The two-sided significance level was set at0.05. Bonferroni correction was applied post hoc withineach set of tabulated results to adjust for the number ofstatistical comparisons made. SAS� Version 8.2 wasused to perform all analyses.

3. Results

There were 153 subjects entered in the study: 107 chil-dren with ADHD and 46 healthy control subjects. Fif-teen children with ADHD discontinued prior to Visit 3due to patient or caregiver decision, one due to physi-

cian decision, one was lost to follow-up, and five failedto meet entry criteria, leaving a total of 85 ADHD sub-jects. Baseline characteristics for the ADHD and healthycontrol groups were similar, although some significantdifferences in gender and prior stimulant use wereobserved (Table 1). Healthy control subjects had virtu-ally no ADHD symptoms as assessed by an averageADHD-RS-IV-PI total score of 2.85, compared withthe ADHD patients’ average score of 37.25 (p < .001).Only ADHD subjects were eligible to participate inPSG. Subjects who volunteered for the PSG studiesdid not differ from those not volunteering in terms ofbaseline characteristics. Overnight PSG recordings forthe 40 ADHD subjects were largely unremarkable com-pared to age norms, and no patient met diagnostic crite-ria for OSA or PLMD [39].

3.1. Actigraphy

Actiwatch malfunctioning and failure to meet the70% compliance criteria specified in the analysis planresulted in the exclusion of six additional subjects, leav-ing a total of 80 ADHD subjects and 45 healthy controlsubjects for data analysis.

The ADHD group did not have significantlyincreased average sleep onset latency, nor was there asignificant difference in night-to-night variability in sleeponset latency between groups. Actual sleep time wasapproximately one-half hour shorter for the ADHDgroup compared with the healthy control group(460.30 vs. 489.39 min, respectively; p = .001; Table 2).There was no significant difference in night-to-night var-iability in actual sleep time between groups. The ADHDgroup had a larger total amount of interrupted sleeptime than the healthy control group (56.70 vs.44.49 min, respectively; p = .002). In contrast, theADHD group experienced a significantly fewer numberof sleep interruptions than the healthy control group(35.33 vs. 44.45, respectively; p < .001).

The difference in bedtimes between groups was notstatistically significant (10:00 p.m. in the ADHD groupvs. 9:57 p.m. in the healthy control group). Within theADHD group, there were no statistically significant dif-ferences on actigraphy variables by ADHD severity orsubtype (Tables 3 and 4). In addition, no significantbetween-group differences were found between ADHDchildren with (n = 37) or without oppositional-defiantdisorder (ODD) (n = 43) on any of the major actigraph-ic sleep parameters.

3.2. Parent and child electronic diaries

Similar to the actigraphy results, child diaries did notindicate a statistically significant difference in time to fallasleep between the two groups; however, children withADHD reported that they ‘‘slept less well” than controls

Table 1Summary of demographics and other patient characteristics for entered patients

Characteristic N Children with ADHD N Healthy control subjects p-Value

Gender n (%) 107 46Female 25 (23.4) 23 (50.0) .002

Male 82 (76.6) 23 (50.0)Origin n (%) 107 46Caucasian 78 (72.9) 42 (91.3) .010Other 29 (27.1) 4 (8.7)Mean age in years (SD) 107 10.2 (2.0) 46 10.3 (2.6) .956Mean body mass index (SD) 105 18.9 (3.1) 45 18.5 (4.1) .366Mean height in cm (SD) 105 141.7 (11.7) 46 138.3 (15.0) .139Mean weight in kg (SD) 107 38.4 (10.2) 45 36.9 (14.6) .419DSM-IV ADHD subtype n (%) 103 NAHyperactive/impulsive 2 (1.9)Inattentive 32 (31.1)Mixed 69 (70.0)Prior stimulant exposure n (%) 106 46No 46 (43.4) 46 (100) <.001

Yes 60 (56.6) 0

Bolded p-values were still significant after Bonferroni correction within the table.Abbreviations: ADHD, attention-deficit/hyperactivity disorder; SD, standard deviation; DSM-IV, Diagnostic and Statistical Manual of Mental

Disorders, Fourth Edition.

Table 2Actigraphy variables, children with ADHD versus healthy controlsubjectsa

Variable Group n Mean SD p-Valued

Sleep onset latencyb ADHD 80 31.44 23.07 .795control 45 32.94 17.39

Actual sleep timeb ADHD 80 460.30 46.86 .001

control 45 489.39 39.22Total sleep intervalb ADHD 80 517.01 46.19 .056

control 45 533.88 40.80Interrupted sleep timeb ADHD 80 56.70 19.64 .002

control 45 44.49 17.93# of sleep interruptions ADHD 80 35.33 12.10 <.001

control 45 44.45 14.41Sleep efficiency ADHD 80 0.84 0.05 .014

control 45 0.86 0.04Bedtime ADHD 80 22:00c 44.83b .889

control 45 21:57c 60.27b

Wake-up time ADHD 80 07:09c 33.14b .017control 45 07:24c 54.49b

Abbreviations: ADHD, attention-deficit/hyperactivity disorder; SD,standard deviation; ANOVA, analysis of variance.

a Imputation criteria: visit level average is imputed if the subject hasmore than 70% non-missing records during the visit interval.

b Measured in minutes.c Measured in military time.d p-Value detecting group difference using an ANOVA model with

terms for investigator and group. Bolded p-values were still significantafter Bonferroni correction within the table.

Table 3Actigraphy variables, Mild/Moderate versus severe ADHDa

Variable Group n Mean SD p-Valued

Sleep onset latencyb Mild/Mod 46 30.57 23.09 .580severe 34 32.62 23.35

Actual sleep timeb Mild/Mod 46 459.27 53.39 .611severe 34 461.71 36.97

Total sleep intervalb Mild/Mod 46 515.02 51.71 .581severe 34 519.69 38.06

Interrupted sleep timeb Mild/Mod 46 55.76 22.57 .876severe 34 57.99 15.03

# of sleep interruptions Mild/Mod 46 35.85 11.96 .961severe 34 34.62 12.43

Sleep efficiency Mild/Mod 46 0.84 0.05 .842severe 34 0.84 0.04

Bedtime Mild/Mod 46 22:00c 48.57b .800severe 34 22:01c 39.93b

Wake-up time Mild/Mod 46 07:05c 34.81b .399severe 34 07:13c 30.72b

Abbreviations: ADHD, attention-deficit/hyperactivity disorder; SD,standard deviation; Mod, moderate; ANOVA, analysis of variance.

a Imputation criteria: visit level average is imputed if the subject hasmore than 70% non-missing records during the visit interval.

b Measured in minutes.c Measured in military time.d p-Value detecting group difference using an ANOVA model with

terms for investigator and group.

J. Owens et al. / Sleep Medicine 10 (2009) 446–456 451

and that they had significantly more difficulty waking inthe morning and were sleepier during the day (Table 5).Parent diaries showed significant differences betweengroups for all of the sleep and evening/morning behav-ior variables, with the ADHD group consistently experi-encing more difficulties than the control group (Table 6).Post hoc analyses for the ADHD group showed signifi-

cant differences on parent diary items by ADHD sever-ity and subtype and by ODD status, with most analysesindicating that patients of combined ADHD subtypehad greater impairment on sleep-related variables thanthose of inattentive subtype; patients with severe ADHDhad greater impairment on sleep-related variables thanthose with mild/moderate ADHD, and patients withcomorbid ODD had greater impairment on sleep-related

Table 4Actigraphy variables, inattentive versus combined ADHD subtypea

Variable Group n Mean SD p-Valued

Sleep onset latencyb Inattentive 25 30.49 18.56 .896combined 53 28.49 17.61

Actual sleep timeb Inattentive 25 465.16 52.29 .706combined 53 459.53 43.98

Total sleep intervalsb Inattentive 25 518.65 46.18 .694combined 53 518.07 45.23

Interrupted sleep timeb Inattentive 25 53.48 19.51 .942combined 53 58.54 19.79

# Of sleepinterruptions

Inattentive 25 35.77 12.07 .338combined 53 34.86 12.23

Sleep efficiency Inattentive 25 0.85 0.04 .824combined 53 0.84 0.04

Bedtime Inattentive 25 21:58c 51.43b .447combined 53 22:01c 42.49b

Wake-up time Inattentive 25 07:07c 36.75b .617combined 53 07:07c 31.08b

Abbreviations: ADHD, attention-deficit/hyperactivity disorder; SD,standard deviation; ANOVA, analysis of variance.

a Imputation criteria: visit level average is imputed if the subject hasmore than 70% non-missing records during the visit interval.

b Measured in minutes.c Measured in military time.d p-Value detecting group difference using an ANOVA model with

terms for investigator and group.

452 J. Owens et al. / Sleep Medicine 10 (2009) 446–456

variables than those without comorbid ODD. Therewere few strong and no clinically meaningful correla-tions between actigraphy variables and diary questions,nor between corresponding parent and child diaryquestions.

4. Discussion

The results of this study of unmedicated children withADHD who had been screened for both primary sleepdisorders and comorbid psychiatric disorders supportthose of previous studies showing increased parental rat-ings of sleep problems compared to children in the con-trol group. Parents of children with ADHD also

Table 5Child diary results

N ADHD mean (SD)

Time to fall asleepa 61 33.19 (24.46)Difficulty getting upb 66 28.70 (17.28)How well did you sleep?c 61 74.63 (17.86)How sleepy do you feel today?d 66 26.93 (17.84)

Note: The relative position marked by each child on a line was scored on aNote: Only those patients with at least 9 diary records during the 14 days aAbbreviations: ADHD, attention-deficit/hyperactivity disorder; VAS, Visual

a 0 = fell asleep right away; 100 = took greater than 30 min to fall asleep.b 0 = very easy; 100 = very hard.c 0 = very badly; 100 = very well.d 0 = not sleepy at all; 100 = very sleepy.e p-Value detecting group difference using an ANOVA model with terms

Bonferroni correction within the table.

reported significantly more problematic behaviors dur-ing mornings, evenings, and bedtimes than did parentsof children in the control group. Furthermore, anincrease in parent-reported, subjectively measured sleepproblems appeared to be associated with severe ADHD(as opposed to mild/moderate), primarily mixed ADHDsubtype (as opposed to inattentive subtype), and withthe presence of comorbid ODD. Compared with thecontrol group, children with ADHD were more likelyto report that sleep quality was compromised, and thisseemed to translate into a perception of reduced daytimealertness, with increased reports of difficulty getting upin the morning and higher levels of daytime sleepiness.

The relatively low correlation between parent-reportand self-report ratings of sleep in this study for boththe control and ADHD groups is similar to findings inother studies comparing subjective sleep complaints asreported by both school-aged children and their parents[26], although at least one study has suggested that thesecorrelations may actually be higher in children withADHD [16]. In those studies, children tended to reportless difficulty falling asleep than parents reported forthem, which is similar to our diary results in which chil-dren with ADHD did not self-report taking significantlylonger to fall asleep than healthy control subjects,whereas parents of children with ADHD reported thattheir children had significantly more difficulty fallingasleep than did parents of healthy control subjects.The differences between ADHD and control groups onactigraphic sleep parameters appeared to be more oftencorrelated with the self-reports than the parent-reports,emphasizing the importance of questioning the school-aged child as well as the caregiver about sleep issues inthe clinical setting.

Findings using objective actigraphic methodologyshowed ADHD was associated with significantly short-ened sleep duration (by almost 30 min on average),which appeared to relate primarily to the combinedinfluence of an increase in interrupted sleep time and

N Healthy controls mean (SD) p-Valuee

46 31.53 (20.23) 0.18346 15.80 (11.44) <0.001

46 82.41 (13.96) <0.001

46 20.85 (14.05) <0.001

scale of 0–100.fter study entry were included.Analogue Scale.

for investigator and group. Bolded p-values were still significant after

Table 6Parent diary results

N ADHD patients mean (SD) N Healthy controls mean (SD) p-Valuea

Difficulty getting child out of bed 60 0.66 (0.57) 44 0.18 (0.23) <.001

Difficulty getting child ready 60 0.99 (0.53) 44 0.12 (0.22) <.001

Arguing or struggling in morning 60 0.54 (0.45) 44 0.10 (0.15) <.001

Irritable in morning 60 0.43 (0.45) 44 0.10 (0.13) <.001

Difficulty doing homework/tasks 51 1.29 (0.53) 44 0.08 (0.18) <.001

Difficulty sitting still at dinner 52 1.06 (0.68) 44 0.07 (0.17) <.001

Difficulty playing quietly in evening 52 1.25 (0.75) 44 0.09 (0.16) <.001

Inattentive/distracted in evening 53 1.36 (0.62) 44 0.09 (0.16) <.001

Arguing/struggling in evening 53 1.10 (0.64) 44 0.19 (0.26) <.001

Irritable/lose temper in evening 53 0.84 (0.62) 44 0.17 (0.20) <.001

Difficulty transitioning in evening 53 1.06 (0.63) 44 0.06 (0.11) <.001

Difficulty getting ready for bed 53 0.85 (0.56) 42 0.14 (0.19) <.001

Difficulty falling asleep 51 1.08 (0.67) 42 0.58 (0.54) <.001

Note: Each question was answered on a scale of 0–4, with 4 representing greatest impairment.Note: Only those patients with at least 9 diary records during the 14 days after study entry were included.Abbreviations: ADHD, attention-deficit/hyperactivity disorder.

a p-Value detecting group difference using an ANOVA model with terms for investigator and group. Bolded p-values were still significant afterBonferroni correction within the table.

J. Owens et al. / Sleep Medicine 10 (2009) 446–456 453

an earlier morning wake-up time rather than a pro-longed sleep onset latency. On average, 15 min worthof the difference in actual sleep time was due to earlierwake time in the ADHD sample. However, we did notspecifically collect data regarding the reasons for indi-vidual wake times (child woke spontaneously, wasawakened by parent or alarm for school, etc), whichmay have differed between the two samples and thuscould have potentially impacted differences in perceivedbehavior and daytime fatigue. Children with ADHDhad more total interrupted sleep time, yet the numberof distinct periods of sleep interruption of at least oneminute were fewer, suggesting that the periods of inter-rupted sleep were longer in duration compared to con-trols. This may account for these children’s subjectiveimpression that they do not sleep as well.

From a methodological standpoint, it should beemphasized that all actigraphic epochs not scored assleep are considered to be part of a wake bout; thesecan be as short as one minute (one epoch), but may beup to or longer than one hour. In normal populations,there is generally a high degree of correlation betweenPSG-defined arousal/wake and actigraphy-defined‘‘wake bouts,” but this may not be true in potentiallyintrinsically restless sleepers, such as children withADHD; thus, we cannot reliably characterize theseepochs as either ‘‘movements” or ‘‘wake.” Furthermore,the actigraphy watches were empirically set at a ‘‘med-ium” movement sensitivity threshold of 40 (range 20to 80); this may tend to over-score movement epochsas wake epochs in hyperactive ADHD children. Thelarge number of sleep interruption periods in both theADHD and control groups (35 and 44, respectively) alsosuggests that these interrupted sleep intervals most likelyrepresent some combination of periods of wakefulnessand increased movement during sleep, and thus may

be viewed as a more general measure of sleep fragmen-tation or discontinuity.

The failure to find objective differences in sleep onsetlatency in children with ADHD, although similar to pre-vious studies, is still somewhat surprising given the fre-quent reports in clinical practice of delayed sleep onsetin these children. It should be noted that sleep onsetlatency tends to be the least reliable sleep parametermeasured by actigraphy [40], and it may be even moreproblematic to reliably distinguish wakefulness fromsleep onset in children who are either hyperactive whileawake, more restless during sleep, or both. However,similar to findings of Owens, Maxim, and colleagues[16], self-reports of increased time to fall asleep werenot more common in the ADHD children than in thecontrol group, suggesting that the children themselvesdo not perceive significant difficulties in falling asleep.This is in contrast to parental ratings of delayed sleeponset in children with ADHD. Given the differences thatparents of children with ADHD reported in problematicevening and bedtime behavior, it is possible that the per-ception of ‘‘difficulty falling asleep” may be based moreon quality of the parent–child interaction in the eveningand at bedtime rather than an absolute increase in timeto fall asleep. However, because we did not objectivelyobserve parent–child interactions, this remainsspeculative.

We also considered the possibility that increasednight-to-night variability in sleep onset latency in chil-dren with ADHD, as has been reported in a few studies,may partially account for the observed discrepancybetween parents’ perception of problematic sleep onsetand normal objective measures of sleep onset latency.In other words, parents may be more likely to recall,and thus report as ‘‘typical,” those nights on which achild has significant bedtime resistance or difficulty fall-

454 J. Owens et al. / Sleep Medicine 10 (2009) 446–456

ing asleep, but these nights are not necessarily capturedin a specific week of actigraphy sleep onset latency datathat are averaged over time. However, we did not find asignificant actigraphic difference in variability in sleeponset latency in the children with ADHD, suggestingthis is unlikely to be the cause.

A final note regarding the sleep onset latency resultsis that we asked subjects to set a regular bedtime andthen maintain a bedtime within a half-hour of this setbedtime. Subjects were allowed to set a weekend bed-time that was a half-hour later than the school-day bed-time. However, this may have inadvertently introduceda sleep hygiene intervention that in itself helped to reg-ularize sleep and reduce sleep onset latency as well aspotentially reduce night-to-night variability [42], andthe ADHD group may have potentially benefited morefrom this intervention than the control group. Bedtimedid not differ significantly between groups, suggestingthat the lack of difference in sleep onset latency betweengroups was not merely a result of the ADHD childrengoing to bed later and thus falling asleep relatively morequickly. Future studies could use PSG to more thor-oughly examine differences in sleep onset latencybetween ADHD and healthy subjects.

4.1. Limitations

The aim of this study was to examine sleep problemsin a sample of children with ADHD while eliminating asmany potential confounds as possible. However, theresults of this study may not be completely generalizableto children with ADHD in the general population. Froma clinical standpoint, studies suggest that most childrenwith ADHD have at least one comorbid psychiatric con-dition (anxiety, depression, conduct disorder, etc) [43],and that most children with ADHD are treated at somepoint with psychotropic medication [44]. Because theseconditions were exclusionary, our study populationmay not ultimately reflect the frequency or severity ofsleep problems seen in the practice setting. However, itshould be noted that from a theoretical point of view,this allowed us to focus on the relationship betweensleep and ADHD per se, without the confounding effectof comorbidities.

Additional limitations of this study include the rela-tively small sample size, the lack of PSG data from allsubjects to rule out primary sleep disorders, and differ-ences in gender distribution between the ADHD andcontrol groups; however, the percentage of boys in theADHD group was typical for ADHD studies. More-over, polysomnographic studies of large samples of chil-dren suggest relatively minor gender differences in sleeparchitecture [45]. Age represents the most significantconfounding variable in regard to sleep patterns overall,and there was no significant age difference between thetwo groups.

4.2. Implications

Results of this study suggest that children withADHD who do not have psychiatric comorbidities orprimary sleep disorders, and who are not taking anypsychotropic medications, do not have a prolongedsleep onset latency compared to controls; although theydo appear to have a significantly shorter sleep duration.Similar to results of several previous studies, our find-ings suggest that children who have ADHD may haveincreased duration of nocturnal movements or frag-mented sleep time, and thus the quality of their sleepmay be compromised. This reduced sleep quality couldcontribute to the increased level of daytime sleepinessreported in our study as well as in several others andcould potentially further exacerbate ADHD symptoms.It also should be noted that both groups of childrenaveraged considerably less sleep on actigraphy (7.7 hin the ADHD group and 8.2 h in the control group)than is generally considered sufficient in this age range,especially in the younger children, emphasizing thatoverall, children may not be getting an adequate quan-tity of sleep, further adding to the burden of neurobe-havioral deficits in those children with ADHD.

These results do not imply that sleep problems in thesechildren do not exist or that, in actual clinical practice, sleepproblems are not a source of significant distress for fami-lies. It is possible, for example, that there are subgroupsof children with ADHD who have specific ‘‘sleep pheno-types” and whose presentation is suggestive of an intrinsicADHD-mediated ‘‘hyperarousal” at bedtime that couldrepresent an alteration of the normal homeostatic sleepdrive, or who have a primary circadian-mediated sleepphase delay, either of which could result in difficulty set-tling. In fact, the distribution of sleep onset time in theADHD group suggests there may be a certain percentageof ‘‘outliers” who have more difficulty falling asleep.

Nonetheless, the findings of this study also suggest thatthe nature of the parent–child interaction and the chil-dren’s problematic behavior, particularly in the eveningand in the time leading up to bedtime, appeared to bethe major issue (rather than sleep onset delay per se)accounting for perceived bedtime problems. Thus, inter-vention in these cases should be targeted toward behav-ioral-management strategies and perhaps towardimproved pharmacologic control of ADHD behaviorsin the evening. It is also important for clinicians to screenfor and mitigate, if not eliminate, those common etiologicfactors, such as comorbid anxiety, dosing level and timingof psychotropic medications, and obstructive sleep apnea,in children with ADHD who present with sleep problems.

Finally, our results support the need for additionalstudies to further elucidate the nature of both the sleepdisturbance and impact on daytime functioning and todetermine optimal treatment strategies for thesechildren.

J. Owens et al. / Sleep Medicine 10 (2009) 446–456 455

Acknowledgments

The authors acknowledge Megan Crouch for hercontributions.

This research was supported by Eli Lilly andCompany.

Within the last 3 years, Dr. Owens has received re-search grant support from Sepracor, Eli Lilly and Com-pany, Cephalon, Johnson & Johnson, Boehringer-Ingleheim, and Shire; has served as a consultant for Shire,Cephalon, Johnson & Johnson, Sanofi-Aventis, McNeil,and Boehringer-Ingleheim; has served on speakers’ bu-reaus for Johnson & Johnson, Eli Lilly and Company,and Sanofi-Aventis; and has served on advisory boardsfor Select Comfort, Eli Lilly and Company, Cephalon,and Pfizer. Within the last 5 years, Dr. Sangal has receivedresearch grant support from Organon, Shire, Merck, Ab-bott, Neurogen, Eli Lilly and Company, Glaxo-Smith-Kline, Cephalon, Sanofi-Aventis, Somaxon, Organon,Novartis, and Takeda. At the time of this research/man-uscript development, Dr. Sutton was a stock shareholderand full-time employee of Eli Lilly and Company; she iscurrently a full-time employee of i3 Research. Drs. Bak-ken, Allen, and Kelsey are stock shareholders and full-time employees of Eli Lilly and Company.

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