Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder, with symptoms that remit or persist over time. Biological mechanisms underlying symptom change remain poorly understood, though epigenetic processes, like DNA methylation (DNAm), may serve as dynamic biomarkers of clinical outcomes. We examined change in DNAm in children and adolescents with and without ADHD, including differences between remitted and persistent ADHD.

We analyzed 219 saliva samples from 94 participants (aged 9.5–14.5 years) attending two to three waves of NICAP (Neuroimaging of the Children’s Attention Project). DNAm was profiled using the Infinium MethylationEPIC BeadChip. Linear mixed models adjusted for age, sex, medication, batch, and cell-proportion assessed longitudinal change. Comparisons included (1) individuals with versus without ADHD, (2) persistent or remitted ADHD versus without ADHD, and (3) persistent versus remitted ADHD. False discovery rate correction controlled for multiple testing (FDR-adjusted-p < 0.05).

Comparison (1) showed null findings after correction for multiple testing. In contrast to those without ADHD (2), the average DNAm was statistically different at 2 sites in persistent ADHD (FDR-adjusted-p < 0.05) and 3 sites in remitted ADHD (FDR-adjusted-p < 0.03), and methylation of 3 additional CpGs differentially changed in persistent ADHD (FDR-adjusted-p < 0.04). Remitted differed from persistent ADHD (3) at 4 CpGs, including cg21443143 (ZFAT), which showed a decline over time. Gene enrichment links findings to brain structures and function, though these did not survive multiple testing.

Our study identified several epigenetic differences between remitted and persistent ADHD outcomes from typical development, and from each other. Given the early stage of this research, our findings warrant further prospective epigenome-wide studies into these diagnostic trajectories.

CHD is the most common congenital anomaly worldwide. Advances in paediatric cardiology and cardiac surgery have transformed survival, shifting attention towards long-term psychosocial adaptation, neurodevelopment, quality of life, and relational well-being for children and their families.

This narrative review examines the psychosocial, developmental, familial, and relational dimensions of childhood CHD. Literature was identified through PubMed, Scopus, and Google Scholar, with thematic synthesis of evidence relating to psychosocial adaptation, parental mental health, neurodevelopment, resilience, belonging, peer relationships, and models of family- and relationship-centred care.

Childhood CHD is associated with repeated hospitalisation, developmental disruption, emotional distress, and lifelong uncertainty, with psychosocial effects extending beyond the child to parents, siblings, grandparents, peers, schools, and healthcare professionals. Families frequently experience anxiety, depression, chronic vigilance, and posttraumatic stress symptoms, while children and adolescents face challenges related to identity, belonging, and social participation. Supportive relationships, multidisciplinary psychosocial care, educational integration, peer support, and developmentally informed interventions may strengthen resilience and improve long-term adaptation. Patients with advanced heart failure requiring ventricular assist devices or heart transplantation, and their families experience additional uncertainty and psychological burden that warrant dedicated psychosocial support.

Psychosocial outcomes in CHD are shaped not only by medical care but also by the quality of the relationships surrounding the child. Relationship-centred care builds upon established family-centred care by recognising the broader relational ecosystem that influences development, resilience, participation, and quality of life. Future paediatric cardiology care should integrate longitudinal psychosocial, developmental, educational, and relational support alongside advances in medical treatment.

Early motor and language milestones are key indicators of neurodevelopment, yet their associations with later autism traits and attention-deficit/hyperactivity disorder (ADHD) symptoms remain poorly understood. Neurobiological mechanisms linking early developmental delays to these conditions are not well established. Here, we investigate associations between early developmental milestones, resting-state functional connectivity (rsFC), and neurodevelopmental traits in a large adolescent sample.

Data were drawn from the Adolescent Brain Cognitive Development study (ABCD) and included 6,663 participants (age range = 8.92–11.08 years; mean age = 9.92 years; 48.42% female). Developmental measures included roll over, sit without assistance, walk without assistance, speech development, gross motor development, and coordination. Autism traits were assessed using the Social Responsiveness Scale, and ADHD symptoms were assessed using the Attention Problems subscale of the Child Behavior Checklist. rsFC was examined within and between cortical and subcortical regions. Linear mixed-effects (LME) models and Bayesian mediation analyses assessed associations between developmental measures, rsFC, and neurodevelopmental traits.

LME models revealed shared and condition-specific associations. Poor coordination was associated with higher autism traits and ADHD symptoms, whereas delayed speech development was associated with autism traits, and delayed walking without assistance with ADHD symptoms. We found negligible evidence that rsFC measures mediated associations between early developmental milestones and neurodevelopmental traits. Indirect effects were modest, accounting for less than 2% of associations with autism traits, although somewhat larger effects were observed for ADHD symptoms.

These findings suggest overlapping developmental pathways, with intrinsic connectivity reflecting downstream neural processes rather than primary mediating mechanisms.

Charting developmental abnormalities in future psychotic disorder could help identify pathogenic processes. Head circumference (HC) is a proxy for brain size. Studies of HC and its developmental trajectories in future psychotic disorder cases and across the psychosis spectrum are inconclusive. It is important to determine whether deviations in HC are specific or reflect a general growth disorder.

We used data from the Avon Longitudinal Study of Parents and Children (ALSPAC) to chart HC trajectories from birth to 15 years in individuals with operationally-defined psychotic disorder (N = 62), psychotic experiences (PE; N = 339) and controls (N = 3,527). We extracted total intracranial volume (TIV) from MRI data on a subset (N = 347) scanned at age 20.

HC at birth, 7 and 15 years was correlated with TIV at age 20 (r’s = 0.45–0.77). The psychotic disorder group had consistently smaller HC from birth through to adolescence (B = −0.26, p = 0.02). Females with PE had smaller HC across childhood and adolescence (B = −0.27, p = 0.016), while males with PE had consistently larger HC (B = 0.35, p = 0.023). The effects did not change when controlling for maternal and pregnancy-related characteristics but attenuated after controlling for height, except in males with PE.

Deviations in head and hence brain size across the psychosis spectrum likely reflect a more general growth abnormality. Future studies should examine factors regulating growth during early life in relation to psychosis, including sex, to understand underlying mechanisms.

Infants with CHD experience feeding disruptions during a critical phase in oral feeding development. Dependency on high respiratory supports interfere with oral feeding opportunities. There is little evidence guiding oral feeding practices for infants requiring high flow nasal cannula and nasal continuous positive airway pressure. The aim of this study was to describe current US institutional feeding practices for infants with CHD on non-invasive ventilation.

This was a cross-sectional survey of clinicians from primarily US institutions that were members of the Cardiac Neurodevelopmental Outcomes Collaborative.

From 35 institutions contacted, 20 (57%) feeding specialists responded. Most institutions (80%) did not utilise formal guidelines for oral feeding introduction on nasal continuous positive airway pressure or high flow nasal cannula. Most institutions (80%) did not allow full oral feeds on nasal continuous positive airway pressure, but 70% centres allowed full oral nutrition on high flow nasal cannula and (85%) allowed small volume oral feeding with specifications for the level of oxygen support. While most respondents (65%) reported feeding assessment completion on all infants both pre and postoperatively, few (30%) institutions utilised a formal cue-based assessment.

Responses indicate that institutions generally do not allow oral feeding on respiratory support above high flow nasal cannula. Most centres do not utilise formal respiratory/cue based assessments to determine infant feeding readiness while on non-invasive ventilation. Future multidisciplinary research and quality improvement initiatives are needed to examine the effects of feeding infants with CHD while on non-invasive ventilation and to develop centre-specific guidelines to direct feeding progression, with potential to improve oral feeding outcomes while supporting multisystem stability.

Children with CHD who have undergone corrective or palliative surgery are at increased risk for developmental delays. One important aspect is the development of emotional intelligence. Although emotional intelligence is not explicitly included in the current neurodevelopmental battery testing, increasing evidence supports the inclusion of it.

In this prospective, single-centre, cross-sectional pilot study, we analysed emotional intelligence in a broad spectrum of English-speaking paediatric patients, aged 7 to 17 years old, with a confirmed CHD and without moderate-to-severe developmental delay. We evaluated emotional intelligence using the Bar-On Emotional Quotient Inventory: Youth Version questionnaire, administered parent questionnaires, and reviewed medical records. We determined associations between components of the Emotional Quotient Inventory: Youth Version and pertinent demographic and clinical variables using one-way ANOVA and multivariable regression.

A total of 67 patients were included in this study; 68.7% underwent cardiac surgery in infancy, 74.2% with cardiopulmonary bypass. Children with greater CHD severity had lower emotional quotient scores, and there was a significant inverse relationship between social vulnerability index scores and emotional quotient scores. Multivariable modelling showed that social vulnerability scores explained 25.1% of emotional quotient total variance. Higher CHD severity, surgical complexity, multiple operations, and higher social vulnerability scores were associated with lower emotional quotient stress and adaptability.

Emotional intelligence is a modifiable component of developmental progression of children with CHD and can provide a complementary perspective of neurodevelopmental functioning. Addition of the Emotional Quotient Inventory: Youth Version to the battery of testing may be considered.

Attention-deficit/hyperactivity disorder (ADHD) involves altered neurodevelopment, yet the underlying mechanisms remain elusive. Aperiodic EEG components may reflect neural functions like excitatory/inhibitory balance, but their age-related differences in ADHD and link to default mode network (DMN) dysfunction are unexplored.

We included 110 medication-naïve children/adolescents with ADHD and 100 matched typically developing peers aged 6–14 years. Aperiodic parameters (exponent, offset) were derived, and source-localized alpha-band DMN coherence was computed. The sample was stratified into middle childhood (6–9 years) and early adolescence (10–14 years) subgroups to delineate age-dependent patterns.

ADHD showed globally increased exponent and offset versus controls. Normative age-related decreases were significantly attenuated in ADHD, indicating divergence from typical development. Age-stratified analyses revealed distinct patterns: in middle childhood, increased frontal offset correlated positively with inattention (right hemisphere) and hyperactivity/impulsivity (left hemisphere); in early adolescence, it associated with reduced coherence in two DMN pathways (right mSFG–left hippocampus and left mSFG–right MTG).

Aperiodic activity differences in ADHD are age-dependent. Younger children exhibit focal, symptom-linked frontal abnormalities, whereas adolescents show pervasive network-level dysregulation. Aperiodic measures may capture age-varying ADHD pathophysiology, informing developmentally targeted biomarkers.

This scoping review evaluates the physiological, neurodevelopmental, and psychosocial effects of reading interventions on critically ill infants and young children.

Critically ill children, including premature infants and those with critical CHDs, are at elevated risk for neurodevelopmental complications that may be exacerbated by noxious stimuli in hospital settings. Given the increased awareness of the significance of developmental care in the critical care environment and the well-established role of reading and literacy interventions in healthy children, a potential method to improve developmental outcomes for critically ill children is early promotion of literacy. We reviewed reading-based interventions in critical care settings using a scoping review framework.

Searches were performed in clinical literature databases for articles evaluating outcomes consequent to or co-occurring with any neonatal or paediatric intensive care setting intervention involving reading to a child. Data and textual content extracted included measures of child physiological status, length of stay, acuity, stress/pain, health status, quality of life, neurodevelopment, as well as parent psychosocial and emotional functioning.

This review identified multiple potential benefits of reading to critically ill children at the bedside, including improved physiological and early literacy outcomes for paediatric patients as well as heightened senses of self-efficacy and psychological well-being for parents. Due to the observed positive impact and lack of negative effects, current literature about reading interventions in critical care settings indicates that such programmes are likely to be a scalable, inexpensive option for facilitating neurodevelopment and bonding for children and their families.

Few studies have quantitatively characterised the shared and distinct features of the epigenetic age signature of schizophrenia, bipolar disorder and major depressive disorder.

To construct a multi-platform epigenetic clock tailored to human blood and brain tissues, and to characterise variations in epigenetic age acceleration across these three common psychiatric disorders.

We integrated 31 publicly available DNA methylation data-sets generated on the platforms Illumina 27K, 450K and EPIC (850K) from patients with schizophrenia, bipolar disorder or major depressive disorder, and from matched controls. Using elastic net regression combined with sure independence screening, we developed the blood–brain clock and applied it to assess disorder-specific epigenetic age acceleration in blood and brain.

The blood–brain clock achieved high accuracy across tissues and outperformed established predictors, particularly in brain samples. Epigenetic age acceleration was reduced in schizophrenia, increased in bipolar disorder and major depressive disorder and strongly elevated in Alzheimer’s disease (positive control). Alterations appeared earlier in blood than in brain. Meta-analysis confirmed that both reduced acceleration (schizophrenia) and increased acceleration (bipolar disorder, major depressive disorder, Alzheimer’s disease) were significantly associated with disease prevalence. Differential methylation analyses further revealed that the blood–brain clock probes captured disease-associated signals, with schizophrenia showing the greatest overlap with causal risk loci, and opposite methylation patterns distinguishing schizophrenia from bipolar disorder or major depressive disorder. A subset of blood DNA methylation probes enabled high-precision classification between schizophrenia and bipolar disorder or major depressive disorder.

This blood–brain clock reveals distinct patterns of epigenetic age acceleration across psychiatric disorders, reflecting disorder-specific and shared biological ageing signatures. The manifestation of these alterations in peripheral blood highlights its potential as a non-invasive biomarker for early detection, risk stratification and differential classification of schizophrenia, bipolar disorder and major depressive disorder.