Attention Deficit Hyperactivity Disorder (ADHD) is a prevalent neurodevelopmental disorder in children. Abnormalities in sleep metrics among ADHD children gradually garnered attention. However, whether significant differences existed in sleep metrics between ADHD children and their typically developing (TD) counterparts remained controversial, with inconsistent conclusions across studies. Furthermore, the potential moderating effects of age and gender on these differential patterns remained insufficiently characterized.

The current study systematically analyzed multimodal sleep monitoring data (polysomnography, actigraphy, electroencephalography, and questionnaires) from 34 articles spanning three decades (44 independent studies: 2,239 ADHD children vs. 57,181 TD children), focusing on core sleep metrics (total sleep time, sleep efficiency, sleep latency, wake after sleep onset, awakening index, and stage shifts) and their complex moderating mechanisms.

The results demonstrated that ADHD children exhibited impaired sleep continuity (reduced total sleep time, increased stage shifts), severe sleep interruption (prolonged wake after sleep onset, elevated awakening index), and abnormal sleep process effectiveness (decreased sleep efficiency, extended sleep latency). Demographic analyses revealed that maturation exacerbated ADHD-related sleep deficits, and male ADHD children had more severe sleep problems than female ADHD children. Furthermore, the moderating effect of gender composition on the awakening index showed interaction effects with other sleep metrics. In addition, slow-wave sleep acted as both a moderator and mediator in group differences of the awakening index.

These findings provided novel neurodevelopmental explanations for sleep dysregulation in ADHD and proposed clinically translatable strategies involving gender-specific interventions and neuromodulation targeting slow-wave sleep.

Healthy sleep contributes to better cognitive functioning in children. This study sought to investigate the role of pre-injury sleep disturbance as a predictor or moderator of cognitive functioning across 6 months post-injury in children with mild traumatic brain injury (mTBI) or orthopedic injury (OI).

Participants were 143 children with mTBI and 74 with OI, aged 8 – 16 years, prospectively recruited from the Emergency Departments of two children’s hospitals in Ohio, USA. Parents rated their children’s pre-injury sleep retrospectively using the Sleep Disorders Inventory for Students. Children completed the National Institutes of Health (NIH) Toolbox Cognition Battery at 10 days and 3 and 6 months post-injury.

Group differences in both overall performance and reaction time on the Flanker Inhibitory Control and Attention Test varied significantly as a function of the level of pre-injury sleep disturbance as well as time since injury. At the 10 day visit, among children with worse pre-injury sleep, mTBI was associated with slower reaction times relative to OI. Among children with worse pre-injury sleep, those with mTBI improved over time while those with OI did not. Main effects of pre-injury sleep and time since injury were found for several other NIH Toolbox subtests, with poorer performance associated with worse pre-injury sleep and early vs. later timepoints.

These results suggest that pre-existing sleep disturbances and mTBI are jointly associated with poorer executive functioning post-injury. Interventions to improve sleep might help mitigate the effects of mTBI on children’s cognitive functioning.

Insomnia disorder, characterized by chronic sleep disruption, often co-occurs with maladaptive emotional memory processing. However, much remains unknown regarding the evolution of emotional memories and their neural representations over time among individuals with insomnia disorder.

We examined the electroencephalographic (EEG) activities during emotional memory encoding, post-encoding sleep, and multiple retrieval phases – including immediate post-encoding, post-sleep, and a 7-day delayed retrieval – among 34 participants with insomnia disorder and 35 healthy control participants.

Healthy controls exhibited adaptive dissipation of emotional memory: memory declined over time, accompanied by reduced subjective feelings toward negative memories. In contrast, participants with insomnia exhibited impaired dissipation: they retained both the emotional content and affective tone of the memories, with diminished time-dependent declines in memory and affect. Beyond behavioral performance, only participants with insomnia maintained stable neural representations of emotion over time, a pattern absent in healthy controls. Additionally, during the post-encoding sleep, slow-wave sleep (SWS), and rapid eye movement (REM) sleep durations predicted the adaptive dissipation of emotional memory over time, but only among healthy participants.

These findings highlight abnormalities in emotional memory processing among individuals with insomnia disorder and underscore the important function of SWS and REM sleep in facilitating adaptive emotional memory processing.

Cognitive behavioural therapy for fatigue (CBT-F) and insomnia (CBT-I) are effective therapies. Little is known on their effectiveness when severe fatigue and insomnia co-occur.

This observational study investigated whether the co-occurrence of fatigue and insomnia influences the outcomes of CBT-F and CBT-I. Furthermore, it was determined if changes in fatigue and insomnia symptoms are associated, and how often the co-occurring symptom persists after CBT.

Patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS, n = 241) received CBT-F and patients with insomnia disorder (n = 162) received CBT-I. Outcomes were fatigue severity assessed with the subscale of the Checklist Individual Strength (CIS-fat) and insomnia severity assessed with the Insomnia Severity Index (ISI). In each cohort, treatment outcomes of the subgroups with and without co-occurring symptoms were compared using ANCOVA. The association between changes in insomnia and fatigue severity were determined using Pearson’s correlation coefficient.

There were no differences in treatment outcomes between patients with and without co-occurring fatigue and insomnia (CBT-F: mean difference (95% CI) in CIS-fat-score 0.80 (−2.50–4.11), p = 0.63, d = 0.06; CBT-I: mean difference (95% CI) in ISI-score 0.26 (−1.83–2.34), p = 0.80, d = 0.05). Changes in severity of both symptoms were associated (CBT-F: r = 0.30, p < 0.001, CBT-I: r = 0.50, p < 0.001). Among patients no longer severely fatigued after CBT-F, 31% still reported insomnia; of those without clinical insomnia after CBT-I, 24% remained severely fatigued.

CBT-F and CBT-I maintain their effectiveness when severe fatigue and insomnia co-occur. Changes in severity of both symptoms after CBT are associated, but the co-occurring symptom can persist after successfully treating the target symptom.

Adenoid hypertrophy contributes to nasal obstruction and obstructive sleep disorders in children, but can be difficult to assess. This study examines whether inferior turbinate hypertrophy can predict adenoid hypertrophy severity in children with obstructive sleep disorders.

This retrospective cohort study included children (0–18 years) with a diagnosis of obstructive sleep-disordered breathing or obstructive sleep apnoea who underwent drug-induced sleep endoscopy. Analyses explored demographic, clinical and endoscopic associations with adenoid hypertrophy.

A total of 269 children were included. Separate univariate analyses showed that older age and greater inferior turbinate hypertrophy predicted greater adenoid hypertrophy (p < 0.05). However, in multivariate ordered logistic regression, only inferior turbinate hypertrophy remained significant (p < 0.01), while age did not (p = 0.11).

These findings suggest inferior turbinate hypertrophy may serve as a proxy for adenoid hypertrophy, aiding clinicians in assessment and guiding further evaluation or intervention.