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.

Infants with CHD who undergo cardiopulmonary bypass surgery are at risk of impaired growth and neurodevelopment. However, few studies have thoroughly investigated the risk factors for growth and neurodevelopmental impairments, particularly with respect to the timing of the initial surgical intervention.

We retrospectively analysed term singleton infants with CHD who underwent cardiopulmonary bypass surgery at a Japanese tertiary centre between 2015 and 2021. Neurodevelopment was assessed at 18–22 months of age using the Kyoto Scale of Psychological Development. We compared outcomes by CHD type (univentricular [UV] vs. biventricular [BV]) and analysed risk factors for growth impairment (weight and height < tenth percentile) and neurodevelopmental impairment (developmental quotient [DQ] < 85), including birth weight, sex, the type of CHD (UV or BV), and timing of the initial cardiopulmonary bypass surgery (<28 days or ≥28 days).

Of the 108 eligible children, 29 had UV physiology and 79 had BV physiology. Both groups showed impaired growth, with significantly lower body weights in the UV group. Neurodevelopmental scores (total DQ) were significantly lower in the UV group. Neurodevelopmental impairment (total DQ < 85) was observed in 44/108 (40.7%) children, and after adjustment, UV repair was significantly associated with neurodevelopmental impairment (adjusted odds ratio [OR] 3.11, 95% confidence interval [CI] 1.27–7.65). Timing of the initial cardiopulmonary bypass surgery was not associated with outcomes.

Infants with CHD in Japan exhibit impaired growth and neurodevelopment at 18–22 months following cardiopulmonary bypass surgery, especially those with UV physiology.

This study aimed to evaluate school-age neurodevelopmental outcomes among children with single ventricle heart disease who underwent neonatal Norwood operation with regional cerebral perfusion compared to deep hypothermic circulatory arrest. Additionally, we aimed to identify predictors of school-age development, including early developmental measures.

Patients enrolled in a prospective randomised trial of infants with single ventricle heart disease undergoing the Norwood operation with either regional cerebral perfusion or deep hypothermic circulatory arrest were included. For the same cohort of patients, this study performed neurodevelopmental testing at 5 years and 10 years of age. At 5 years, a comprehensive neuropsychological evaluation was performed. At 10 years, parent report instruments were used to measure participants’ behaviour and executive function.

Forty-one patients at 5 years of age and 33 patients at 10 years of age completed neurodevelopmental evaluation. There were no significant differences in neurodevelopmental scores between the regional cerebral perfusion and deep hypothermic circulatory arrest groups at either 5 or 10 years. At 5 years of age, the average full scale intelligence quotient (IQ) was 93.4 ± SD18.8. The Bayley Scale of Infant Development Psychomotor Developmental Index (r = 0.68, p < .0001) and mental developmental index (r = 0.64, p < .0001) at 1 year positively correlated with the full scale IQ at 5 years.

Neurodevelopment is delayed in patients with single ventricle heart disease. Neurodevelopmental outcomes at school age did not differ based on the perfusion strategy for the Norwood operation. Mental and psychomotor developmental indices at 1 year are predictive of early school-age measures.

Individuals with a family history of bipolar disorder are at increased risk of developing affective psychopathology. Longitudinal imaging studies in young people with familial risk have been limited, and cortical developmental trajectories in the progression towards illness remain obscure.

To establish high-resolution longitudinal differences in cortical structure that are associated with risk of bipolar disorder.

Using structural magnetic resonance imaging data from 217 unrelated ‘Bipolar Kids and Sibs study’ participants (baseline n = 217, follow-up n = 152), we examined changes over a 2-year period in cortical area, thickness and volume, measured at each vertex across the cortical surface. Groups comprised 105 ‘high-risk’ participants with a first-degree relative with bipolar disorder (female n = 64; age in years: M (mean) = 20.9, s.d. = 5.5) and 112 controls with no familial psychiatric history (females n = 60; age in years: M = 22.4, s.d. = 3.7).

Accelerated thickness and volume reductions over time were observed in ‘high-risk’ individuals across multiple cortical regions, relative to controls, including right lateral orbitofrontal thickness (β = 0.033, P < 0.001) and inferior frontal volume (β = 0.021, P < 0.001). These differences were observed after controlling for age, sex, ancestry, current medication status, lifetime psychiatric diagnoses and measures of gross brain morphology.

Longitudinal group differences suggest the presence of thicker cortex in familial ‘high-risk’ individuals at earlier developmental stages, followed by accelerated thinning towards the typical age of bipolar disorder onset. Future examination of genetic and environmental components of familial risk and the mechanistic nature (pathological or protective) of cortical-trajectory differences over time may facilitate the identification of prodromal biomarkers and opportunities for early clinical intervention.

Maternal depressive symptoms can influence brain development in offspring, prenatally through intrauterine programming, and postnatally through caregiving related mother–child interaction.

The participants were 5-year-old mother–child dyads from the FinnBrain Birth Cohort Study (N = 68; 28 boys, 40 girls). Maternal depressive symptoms were assessed with the Edinburgh Postnatal Depression Scale (EPDS) at gestational week 24, 3 months, 6 months, and 12 months postnatal. Children’s brain imaging data were acquired with task-free functional magnetic resonance imaging (fMRI) at the age of 5 years in 7-min scans while watching the Inscapes movie. The derived brain metrics included whole-brain regional homogeneity (ReHo) and seed-based connectivity maps of the bilateral amygdalae.

We found that maternal depressive symptoms were positively associated with ReHo values of the left amygdala. The association was highly localized and strongest with the maternal depressive symptoms at 3 months postnatal. Seed-based connectivity analysis did not reveal associations between distal connectivity of the left amygdala region and maternal depressive symptoms.

These results suggest that maternal depressive symptoms soon after birth may influence offspring’s neurodevelopment in the local functional coherence in the left amygdala. They underline the potential relevance of postnatal maternal distress exposure on neurodevelopment that has received much less attention than prenatal exposures. These results offer a possible thus far understudied pathway of intergenerational effects of perinatal depression that should be further explored in future studies.

Children with heart conditions, particularly CHDs, may experience adverse neurodevelopmental and psychosocial outcomes. Our study aimed to: (1) compare national prevalence of mental, behavioural, and developmental disorders among children by heart condition status and (2) identify associated characteristics among children with heart conditions.

Nationally representative data from the National Survey of Children’s Health (2016–2021) on U.S. children aged 6–17 years without Down syndrome were analysed. Caregivers reported whether a healthcare provider told them their child has ever had a heart condition or currently has depression, anxiety, ADHD, behavioural, or conduct problems, Tourette syndrome, autism spectrum disorder, developmental delay, intellectual disability, learning disability, or a speech or other language disorder. Logistic regression analysis compared disorder prevalence by heart condition status and, among children with heart conditions, assessed whether disorders were associated with demographic and contextual characteristics.

Among 3,440 children with heart conditions, 42% had an examined disorder, compared to 23% of 133,280 children without heart conditions (adjusted prevalence ratio = 1.8; 95% confidence interval: 1.7, 2.0). Each disorder was more prevalent among children with versus without heart conditions (adjusted prevalence ratio range: 1.9 to 5.1), with anxiety (22.1%), ADHD (20.4%), and learning disabilities (19.6%) most common. Among children with heart conditions, disorders were consistently associated with an increased number of adverse childhood experiences.

These findings support clinical guidelines recommending neurodevelopmental and mental health screening and interventions for children with heart conditions and can be used as a national baseline to gauge progress of guideline implementation.

“Frailty” is associated with worse outcomes in adult cardiology. There is limited data on the associations between frailty and outcomes in paediatric cardiology. We aimed to define the prevalence of frailty and identify associations between frailty and neurodevelopmental and quality-of-life outcomes in high-risk paediatric cardiac populations.

This cross-sectional study included patients 4–18 years seen in a neurodevelopmental programme between 6/2017 and 11/2022. Demographic and clinical data were obtained from medical records. As part of the routine care, physical therapy assessment and neurocognitive, psychosocial, adaptive functioning, and quality-of-life surveys were administered. Social determinants of health were assessed by insurance status and Childhood Opportunity Index. Frailty was defined as the abnormality in 3 of 5 categories: body composition, weakness, slowness, physical activity, and exhaustion. Chi-Square, Student t, and Wilcoxon Rank Sum tests were used to assess differences between frail and non-frail groups.

Of the 270 patients, 101 (37%) met the frailty criteria. Frailty was not associated with social determinants of health, cardiac diagnosis, genetic syndrome, number of cardiac surgeries, or history of clinical complications. Frail patients were more likely to be older (p = 0.004) and have neurocognitive (p = 0.024), emotional (p = 0.003), social (p < 0.001), motor (p < 0.001), and adaptive dysfunction (p < 0.001) and lower quality of life (p = 0.029).

Frailty is common in school-aged patients with cardiac disease and is associated with adverse neurocognitive, psychosocial, motor, and adaptive outcomes and worse quality of life. Risk stratification for frailty may be a critical evaluation and screening element of high-risk cardiac patients in neurodevelopmental programmes.