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. Author manuscript; available in PMC: 2026 Mar 5.
Published in final edited form as: Sleep Med. 2026 Feb 13;142:108837. doi: 10.1016/j.sleep.2026.108837

Sleep Physiology Associated with Cognitive Disengagement Syndrome in Adolescents with and without ADHD

Jessica R Lunsford-Avery a,*, Andrew D Krystal b, Melissa C Miller c,d, Stephen P Becker c,d
PMCID: PMC12959369  NIHMSID: NIHMS2149747  PMID: 41713203

Abstract

Objective:

Cognitive disengagement syndrome (CDS) is an attentional phenotype characterized by excessive daydreaming and hypoactivity that is distinct from attention-deficit/hyperactivity disorder (ADHD). Emerging research finds poorer sleep functioning to be associated with CDS symptoms, though few studies have used objective sleep methods such as polysomnography (PSG). This multi-informant, multi-method study examines whether PSG-assessed sleep physiology indices and subjective sleep quality/circadian preference are associated with CDS severity in adolescents with and without ADHD.

Methods:

Participants were 62 medication-free adolescents (ages 13–17, 50% female), half with ADHD and half were non-psychiatric controls. Adolescents completed 3 consecutive nights of ambulatory PSG and measures of sleep quality and circadian preference. Parents completed measures of CDS and ADHD severity. Partial Pearson correlations covarying for age, sex, and pubertal status examined sleep physiology, sleep quality, and circadian preference in relation to CDS. Linear regressions explored whether associations differed by group.

Results:

Adolescents with ADHD displayed greater CDS severity than controls. Longer PSG-measured latency to persistent sleep, greater wake after sleep onset and percentage of stage 1 (N1) sleep, and reduced sleep efficiency and total sleep time were associated with greater CDS severity. Poorer subjective sleep quality and greater eveningness were also associated with greater CDS severity. Findings were largely unchanged in sensitivity analyses controlling for ADHD severity. Associations between sleep and CDS did not differ between adolescents with ADHD compared to non-psychiatric controls.

Conclusion:

Although adolescents with ADHD exhibited greater CDS severity than controls, PSG-assessed sleep physiology indices were associated with greater parent-reported CDS symptoms irrespective of diagnostic group. Longitudinal and experimental research is needed to replicate and extend findings.

Keywords: sleep physiology, polysomnography, ADHD, cognitive disengagement syndrome, sluggish cognitive tempo, adolescents

1. Introduction

There is increasing recognition that cognitive disengagement syndrome (CDS) comprises a distinct attentional phenotype that is distinct from attention-deficit/hyperactivity disorder (ADHD) inattentive symptoms.1,2 Characterized by excessive daydreaming, mental confusion, and hypoactivity, there is now clear evidence that CDS is empirically distinct from ADHD symptoms, and a growing body of research also shows CDS to be independently associated with poorer functioning, including increased internalizing symptoms, socio-emotional difficulties, and academic problems in both children and adults.3–5 Given the personal costs of CDS, better understanding of biological processes related to CDS may open new opportunities for understanding of the underpinnings of the syndrome as well as novel intervention opportunities.

Poor sleep health is a critical transdiagnostic risk factor for a range of psychiatric conditions, cognitive deficits, and adverse functional outcomes,6 and thus is of interest for furthering understanding of CDS. A small but growing body of research has examined the relation between CDS and sleep functioning.5 The vast majority of these studies have relied on subjective ratings of sleep. These studies have found greater CDS symptom severity to be associated with more sleep difficulties, including poorer sleep quality, greater sleep problem severity, and daytime sleepiness.7–11 Longitudinal work suggests sleep problems may predict later CDS symptoms, but not vice versa.12 Evidence suggests that youth with ADHD and co-occurring CDS symptoms have more sleep problems than youth with ADHD only.9,11 Experimental studies have also found adolescents’ CDS symptoms to be worse during restricted compared to healthy sleep duration,13 including in adolescents with ADHD.14 However, much of this research relies on ADHD-only clinical samples, use of CDS measures that lack strong psychometric properties, and heavy reliance on caregiver report. Given that caregivers become less accurate reporters of sleep problems following the transition to adolescence,15,16 adolescent self-report of sleep and use of well-validated CDS measures are critical for clarifying these associations.

Moreover, only two studies have examined objective sleep indices in relation to CDS symptoms. In a sample of early adolescents (ages 12–14) with and without ADHD, higher self-reported CDS symptoms were independently associated above and beyond ADHD symptoms with later sleep onset and shorter sleep duration per actigraphy, but CDS symptoms were not associated with wake time, sleep efficiency, or wake after sleep onset.17 The sole study to examine CDS and polysomnography (PSG)-assessed parameters was conducted in a population-based sample of children ages 6–12 years.18 Although parent-reported sleep problems were associated with CDS symptoms, none of the 14 PSG parameters assessed were related to CDS symptom severity.18 However, this study used a brief (6-item) measure of CDS symptoms, children underwent a single night of PSG with a parent present in a clinical sleep research center, and, as noted by the authors, it is important to examine PSG parameters and CDS in adolescents given possible developmental differences and in naturalistic environments (i.e., at home).

Finally, there is preliminary indication that chronotype may be associated with higher CDS symptom severity. Studies in early adolescents (ages 12–14)17 and adults19,20 have found significant associations between greater preference for eveningness and higher CDS symptoms. The current study aims to extend these findings by examining circadian preference and CDS symptoms in adolescents spanning a wider age range, which is especially important to examine in adolescents given normative circadian phase delays during this developmental period.21

The current study is the first to examine the relationship of sleep and CDS symptoms using PSG in adolescents and in the home setting. It uses a multi-informant, multi-method approach to examine the relation between sleep and CDS symptoms. Using a sample of adolescents with and without ADHD, we examined gold-standard PSG sleep physiology parameters (primary outcomes) in addition to adolescent-reported sleep quality and circadian preference (secondary outcomes) in relation to parent-reported CDS symptom severity. Based on prior work using subjective sleep measures, we expected that shorter PSG-measured sleep duration and more fragmented sleep (greater wake after sleep onset, poorer sleep efficiency), poorer self-reported sleep quality, and greater eveningness preference would be associated with more severe parent-reported CDS symptom severity. We also explored whether any associations between sleep and CDS differed for adolescents with or without ADHD.

2. Methods

2.1. Participants and Procedures.

Detailed study procedures are described elsewhere,22 and were approved in full by the Duke Health IRB. In brief, 62 adolescents between the ages of 13 and 17 (31 with ADHD, any presentation and 31 non-psychiatric controls (NPC)) participated in a gold-standard diagnostic screening visit in which written consent (parent or guardian) and assent (adolescent) were obtained, and the presence or absence of ADHD was established by a PhD-level clinician. Potential NPC participants were excluded if they met criteria for any DSM-5 diagnosis,23 and potential ADHD participants were excluded if they met criteria for any DSM-5 diagnosis other than ADHD and oppositional defiant disorder (ODD). Sleep-promoting (e.g., benzodiazepines, benzodiazepine receptor agonists, antihistamines) and psychotropic medications were excluded in both groups; participants with ADHD taking stimulants or melatonin completed a washout (48 hours and 7 days, respectively) prior to the sleep assessment and remained off these medications for the study duration.

Following screening and washout (if applicable), all participants completed three consecutive nights of ambulatory polysomnography (PSG) during a typical school week (Monday, Tuesday, and Wednesday). They were requested to maintain their habitual sleep patterns during this assessment. Each evening, PSG devices (Alice PDx, Philips Respironics) were attached by a Registered Polysomnographic Technologist at the laboratory. Adolescents then slept at home, removed the devices each morning, and completed a standardized sleep diary.24 On the following day (Thursday), the family returned to the lab for a follow-up visit and completed a range of clinical measures, including self-reports of sleep quality and chronotype and a parent report of CDS symptom severity.

2.2. Measures.

A detailed description of the sleep assessment protocol has been published.22 Briefly, PSG was recorded using a standard montage of 2 EEG channels (C3-O2, C4-O1), 2 eye movement detection (electrooculogram) channels, and a submental electromyogram channel. On night 1 only, screening for arousals associated with possible obstructive sleep apnea and restless legs syndrome was conducted using anterior tibialis electromyogram channels, an airflow channel, and electrocardiogram. Each PSG record was scored using standard scoring criteria25 by highly experienced Registered Polysomnographic Technicians, and variables of interest included percentages of the night spent in sleep stages (stage 1 [N1], stage 2 [N2], stage 3 [N3], rapid eye movement [REM]), latency to REM sleep in minutes, latency to persistent sleep (LPS = time to 10 minutes of continuous sleep), total sleep time (TST = total minutes asleep between sleep start and sleep end), wake after sleep onset (WASO = minutes awake between sleep start and sleep end), and sleep efficiency (SE = TST/time in bed). PSG measures were averaged over 3 nights, which is consistent with prior literature suggesting that PSG indices, when assessed across 3 consecutive nights and averaged, are stable and reflect an individual’s habitual sleep.26 In the parent study using the current sample, only reduced N3% and greater N2% were found to distinguish the ADHD group from non-psychiatric controls (ps <.001).22 Self-reported sleep quality was assessed via the widely-used Pittsburgh Sleep Quality Index (PSQI),27 and self-reported chronotype via the Morningness Eveningness Scale for Children (MESC).28

CDS was assessed using the widely-used, parent-report Barkley Sluggish Cognitive Tempo Scale for Children and Adolescents (BSCTS-CA).29 The 12-item BSCTS-CA queries CDS behaviors, such as daydreaming, mental fog, lethargy, underactivity, apathy, and sluggishness. Each item is rated on a 4-point scale (1=Never/Rarely to 4=Very Often). Total scores range from 12–48, with higher scores indicating greater CDS severity. This scale was associated with good internal consistency and test-retest reliability in a nationally representative sample.30 The scale similarly displayed good internal consistency in the current sample (Cronbach’s α = .89).

2.3. Data Analysis.

Partial Pearson correlations evaluated the associations between PSG-measured sleep indices, self-reported sleep quality and chronotype, and parent-reported CDS and covaried for age, sex assigned at birth, and pubertal status31 in the full sample. A follow-up sensitivity analysis additionally controlled for parent-reported ADHD symptoms (Conners-3 Global ADHD Index),32 and a second sensitivity analysis assessed relationships between PSG-measured sleep indices and parent-reported CDS severity after removing two sleep-related items from the CDS outcome measure (i.e., “has trouble staying alert or awake” and “Seems drowsy, or has a sleepy appearance”). Exploratory linear regressions covarying for age, sex assigned at birth, and pubertal status further explored whether relationships between PSG-sleep variables and CDS differed by group. For each exploratory model, group status (ADHD versus control), the PSG sleep variable of interest, and covariates were entered into step 1 to facilitate interpretation of main effects of group and the PSG variable of interest on CDS severity, and a group by PSG sleep variable interaction was entered into step 2.

3. Results

3.1. Demographics.

Average age of participants was 15.3 (SD=1.4), and 50% were assigned female sex at birth. The majority identified as White race (74%) and non-Hispanic ethnicity (82%). There were no significant differences in demographics across groups (ps>.05). Within the ADHD group, 19 (61%) had a diagnosis of ADHD combined presentation and 12 (39%) had a diagnosis of ADHD predominantly inattentive presentation; 4 (13%) had a comorbid ODD diagnosis. No participants in either group exceeded arousal screening cutoffs (Apnea Hypopnea Index > 5, Periodic Leg Movement Arousal Index > 10).

3.2. Group differences in CDS Severity.

Parent-rated CDS symptom severity was higher among adolescents with ADHD (M=22.19, SD=6.14) compared to non-psychiatric controls (M=14.48, SD=2.46) (β = .64, t=6.18, p<.001) after accounting for demographic covariates.

3.3. PSG-Measured Sleep and CDS Symptoms in the Full Sample.

Longer LPS, greater WASO and N1%, and reduced SE, N3%, and TST were associated with greater parent-reported CDS in the full sample (ps < .05). In a sensitivity analysis controlling for parent-reported ADHD severity, findings were largely unchanged, except for the N3% result, which was no longer significant, and the finding regarding LPS dropped to a trend level finding. Findings were also largely unchanged in a sensitivity analysis that omitted sleep-related items from the CDS outcome measure, although some previously significant findings (TST, LPS) dropped slightly in significance (i.e., to the trend level). See Table 1.

Table 1.

Associations between Measures of Sleep and Parent-Reported CDS Severity

Sleep Variable Primary Analysis Sensitivity Analysis Covarying for ADHD Sensitivity Analysis Removing Sleep-Related Items
PSG
 TST −.29* −.29* −.26+
 SE −.33* −.37** −.31*
 LPS .28* .23+ .27+
 WASO .31* .37** .32*
 N1% .34* .36** .36**
 N2% .26+ .11 .25+
 N3% −.29* −.13 −.29*
 REM% −.23+ −.24+ −.23
 REM Latency −.09 −.06 −.05
Self-Report
 PSQI .34* .19 .34**
 MESC −.56** −.49** −.55**
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Note:

**

p<.01

*

p<.05

+

p≤.10.

Abbreviations : ADHD=attention-deficit/hyperactivity disorder; CDS=cognitive disengagement syndrome; LPS=Latency to Persistent Sleep; MESC=Morningness Eveningness Scale for Children; N1=Stage 1; N2=Stage 2; N3=Stage 3; PSG=Polysomnography; PSQI= Pittsburgh Sleep Quality Index; REM=Rapid Eye Movement Sleep; SE=Sleep Efficiency; TST=Total Sleep Time; WASO=Wake After Sleep Onset.

3.4. Self-Reported Sleep Quality, Chronotype, and CDS Symptoms in the Full Sample.

Poorer overall self-reported sleep quality on the PSQI was positively related to greater parent-reported CDS symptom severity, and this association remained significant in a sensitivity analysis in which sleep-related items were removed from the CDS outcome measure. The relationship between self-reported sleep quality and CDS severity was in a similar direction, no longer significant, in a sensitivity analysis controlling for parent-reported ADHD severity. Greater eveningness preference was associated with greater parent-reported CDS, and this finding remained significant in sensitivity analyses that either controlled for parent-reported ADHD severity or removed sleep-related items from the CDS outcome measure. See Table 1.

3.5. Group by PSG Sleep Interactions

Exploratory linear regressions modeling each of the PSG variables, group, and covariates in step 1 consistently found significant main effects of group on CDS severity, suggesting that adolescents with ADHD displayed increased CDS severity after accounting for the PSG sleep measure, regardless of the specific PSG variable included. In addition, models examining SE, TST, WASO, and N1% found significant main effects of these PSG variables on CDS severity after accounting for the effect of group on CDS severity. In models assessing LPS, N2%, N3%, REM%, and REM latency, there were no significant main effects of PSG sleep variables on CDS severity in step 1. When group by PSG sleep interactions were added in step 2, no significant interaction effects were observed. See Table 2.

Table 2.

Exploratory Linear Regression Analyses Assessing ADHD Group by PSG Sleep Variable Interactions on CDS Severity

Step 1 (Main Effects) Step 2 (Interaction Effect)
Sleep Variable Group PSG Variable Group*PSG Variable
 TST .63*** −.22* .86
 SE .64*** −.26** .80
 LPS .62*** .15 −.34
 WASO .64*** .21* −.07
 N1% .64*** .26** .25
 N2% .69*** −.04 .17
 N3% .67*** −.001 −.82
 REM% .65*** −.14 .53
 REM Latency .67*** −.05 .69
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Note: All linear régressions control for age, sex assigned at birth, and puberty. Values reflect standardized betas. Significance notations:

***

p<.001

**

p<.01

*

p<.05

Abbreviations : CDS=cognitive disengagement syndrome; LPS=Latency to Persistent Sleep; N1=Stage 1; N2=Stage 2; N3=Stage 3; PSG=Polysomnography; REM=Rapid Eye Movement Sleep; SE=Sleep Efficiency; TST=Total Sleep Time; WASO=Wake After Sleep Onset.

4. Discussion

This study is among the first to use the gold-standard measure of sleep (PSG) to investigate relationships between sleep physiology and CDS symptoms, and the first to do so in adolescents with and without a diagnosis of ADHD and in the home setting. Results from the full sample suggest that shorter, lighter, and more fragmented PSG-measured sleep, as well as greater eveningness preference, were associated with greater CDS symptoms. These relationships were generally found to be robust in sensitivity analyses controlling for ADHD symptom severity or removing sleep-related items from the CDS scale. Although adolescents with ADHD displayed greater CDS symptom severity on average, exploratory analyses did not find evidence of differential associations between sleep physiology and CDS severity by clinical group, potentially suggesting links between sleep and CDS are transdiagnostic. Of note, although reduced proportion of slow wave sleep, greater sleep latency, and poorer subjective sleep quality were found to relate to increased CDS in the full sample, these associations were not found in the sensitivity analysis controlling for ADHD.

Only one previous study examined associations between CDS symptoms and PSG-derived measures of sleep, finding no significant associations.18 In contrast, we found numerous significant associations of PSG measures with CDS symptoms, with several aspects of sleep quality (nocturnal awakenings, reduced sleep efficiency, and greater proportion of the night spent in light sleep) that were significant in primary and sensitivity analyses. There are several reasons why our findings may differ from the previous study18 examining these associations. The previous study18 used a population-based sample of school-aged children, a five-item measure of CDS symptoms, and measured sleep in a lab setting; in contrast, the current study included (1) a sample of adolescents diagnosed with ADHD, (2) a more comprehensive measure of CDS, and (3) sleep measured in a naturalistic setting. It will thus be important for future studies to further examine PSG measures of sleep in relation to CDS, and the possibility that associations differ based on developmental period, sample type, and/or measurement approach used.

The pattern of findings in the present study also point to possible PSG-related differences in relation to CDS compared to ADHD. We found consistent evidence that poorer sleep quality, defined by lighter sleep (more time spent in light sleep and night wakings, contributing to lower sleep efficiency) was consistently associated with CDS severity. It is possible that more fragmented sleep due to spending more time spent awake and in N1 light sleep during the sleep period contributes to the mental confusion, fogginess, and hypoactivity characteristic of CDS. In contrast, no associations were found between percent of time in either N2 or REM sleep, or with REM latency, with CDS, and the initial associations between sleep latency and percent of time in N3 sleep were no longer significant when covarying for ADHD. In contrast, in the primary study involving the same sample,22 adolescents with ADHD had lower percentage of time in N3 and more time in N2 sleep than adolescents without ADHD. In addition, as in the prior CDS-focused study,18 we did not find any association between REM latency and CDS, whereas a recent study of adolescents with ADHD found significantly shorter REM latency in adolescents with ADHD compared to adolescents without ADHD.33 There may thus be subtle but important differences in how sleep physiology relates to the distinct but strongly related psychopathology domains of CDS and ADHD. Of note, these patterns may be similar across individuals who do and do not meet clinical thresholds for ADHD, as we did not find any evidence of moderating effect by group status in the current study of adolescents with and without ADHD. Additional studies with larger samples are warranted, ideally using longitudinal data that can yield a developmentally-informed understanding of the interrelations involving sleep physiology and CDS and ADHD symptoms.

The finding that self-reported sleep quality was significantly associated with caregiver-reported CDS symptoms is consistent with prior research demonstrating a link between CDS and multiple domains of subjectively-reported sleep functioning.34–36 Importantly, this association was significant even when items pertaining to daytime sleepiness were omitted from the CDS outcome measure, providing strong evidence for a significant association between CDS and sleep quality beyond daytime sleepiness. However, this association was not significant when covarying for ADHD symptoms, suggesting there may be unique sleep-related difficulties associated with ADHD and CDS.

Finally, we found consistent evidence that greater eveningness preference was significantly associated with greater parent-reported CDS symptoms, extending previous research that found similar associations among early adolescents aged 12–1436 and adults.37–39 These consistent findings across sample types and developmental periods provide important replication pointing to the need for additional research examining the roles of sleep and circadian function as correlates, contributors, or interacting factors in relation to the CDS phenotype. In particular, well-powered studies utilizing larger samples and multi-modal sleep and circadian assessments (e.g., PSG, chronotype preference, and dim light melatonin onset [DLMO] protocols) are critical for disentangling sleep versus circadian influences, as well as potential interactive effects, on CDS. In addition, given the consistent association between CDS and sleep functioning, sleep and circadian interventions may be a promising direction for future research examining treatment of CDS.40

Limitations of the current study are important to consider. First, despite assessment of sleep functioning across multiple days, we are unable to determine directionality or mechanisms of the association between CDS and sleep functioning. Second, our study relied exclusively on parent-report to assess CDS symptoms, which may not sufficiently capture symptoms or impairment across settings. Third, our sample was relatively small and predominantly White. Fourth, our protocol did not account for the potential effects of caffeine use on findings. Future research should aim to extend these findings utilizing longitudinal methods, additional informants (i.e., self-report, caregiver-report), and a larger, more heterogenous sample. Future research that builds on the current study findings will be important to further clarity the similar and distinct associations sleep and circadian factors have in relation ADHD vs. CDS, and to determine if treatments aimed at improving sleep and circadian function have promise as a means to improve CDS.

Highlights.

  • Physiological sleep correlates of cognitive disengagement syndrome (CDS) are unknown.

  • Polysomnography-measured sleep and CDS were examined in teens with and without ADHD.

  • Disrupted latency, awakenings, N1, efficiency, and duration related to CDS in teens.

  • Relationships between sleep physiology and CDS did not differ between groups.

  • Longitudinal and experimental research is needed to replicate and extend findings.

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