Sleep disorders are highly prevalent in children with Autism Spectrum Disorder (ASD), profoundly impacting their neurodevelopment and daily functioning. Alterations in sleep architecture and regulatory mechanisms contribute to difficulties with sleep onset, maintenance, and overall sleep quality. Sensory processing differences, commonly observed in ASD, may further exacerbate these disturbances by affecting arousal regulation and environmental responsiveness during sleep. Given the fundamental role of sleep in brain maturation, its disruption negatively impacts synaptic plasticity and neurological development, particularly during critical periods. These sleep-related alterations can influence cognitive and behavioral outcomes and may serve as early indicators of ASD, highlighting their potential value in early diagnosis and intervention. Understanding the neurobiological mechanisms linking sleep and ASD is essential for developing targeted therapeutic strategies. Ongoing research increasingly focuses on pharmacological, nutraceutical, and behavioral interventions aimed at mitigating sleep disorders and their cascading effects on neurodevelopment. Optimizing these therapeutic approaches through a multidisciplinary lens is crucial for enhancing clinical outcomes and improving overall quality of life in children with ASD.

Autism spectrum disorder (ASD) is a complex neurodevelopmental condition with multifactorial origins, including the potential involvement of neurotrophins and growth factors. These molecules, which are crucial for neuronal survival, synaptic plasticity, and brain development, have been implicated in ASD pathophysiology. Altered levels of neurotrophins such as NGF, BDNF, NT3, and NT4, as well as growth factors like IGF1, VEGF, and FGF, have been associated with cognitive deficits, sensory processing abnormalities, and behavioral issues in ASD patients. However, the literature presents conflicting results, often due to differences in research methodologies, sample sizes, patient populations, and diagnostic criteria. Despite these inconsistencies, the potential of neurotrophins and growth factors as biomarkers and therapeutic targets for ASD remains promising. Future research with standardized methodologies, larger cohorts, and a clearer understanding of genetic influences is needed to further elucidate their roles in ASD diagnosis and treatment.

Developmental and epileptic encephalopathies (DEEs) represent the most severe group of epilepsies, characterized by drug-resistant seizures, frequent occurrence of epileptiform activity, developmental delay or cognitive impairment. Recent insights have reframed DEEs from static, genetically determined conditions to dynamic disorders with complex and evolving pathophysiology. Several recent studies suggest a link between epilepsy and neurodegeneration, with increased neuronal excitability preceding seizures in conditions characterized by abnormal protein aggregation. Neurodegeneration, defined as the selective and progressive loss of neuronal cells leading to cognitive and functional decline, underlies many progressive neuronal diseases. Although neurodegeneration biomarkers are widely recognized as markers of disease progression in adults, their role in children is still poorly defined and at times controversial. This narrative review aims to summarize current knowledge on the relationship between epilepsy and neurodegeneration, with a focus on potential biomarkers and their implications for disease mechanisms and progression.

Background: The COVID-19 pandemic and related containment measures profoundly affected child and adolescent mental health, with increasing evidence of a rise in psychiatric symptomatology and healthcare burden. This study aimed to evaluate temporal changes in neuropsychiatric presentations before, during, and after the COVID-19 pandemic in a pediatric clinical population. Methods: In this retrospective single-center study, 505 children and adolescents referred to a pediatric neuropsychiatry service were included and stratified into three periods: pre-pandemic (n = 112), pandemic (n = 231), and post-pandemic (n = 162). Clinical and healthcare-related variables were retrospectively collected, including reasons for referral, psychiatric diagnoses, premorbid conditions, and pharmacological treatments. Comparative analyses were performed to identify temporal variations in psychopathological profiles and clinical management. Results: A significant increase in psychiatric symptomatology emerged in the post-pandemic period compared with the pre-pandemic period. In particular, eating disorders, mood disturbances, self-harm, and somatic symptom presentations showed a marked increase over time, presenting as recurrent and associated phenotypes that peaked or consolidated after the acute emergency. The pandemic period was primarily characterized by a greater need for psychopharmacological intervention, specifically driven by the clinical need to manage acute behavioral crises. Overall, findings indicated a persistent increase in the complexity and severity of neuropsychiatric presentations beyond the acute phase of the pandemic. Conclusions: The COVID-19 pandemic was associated with substantial changes in pediatric neuropsychiatric presentations and treatment needs. The persistence of the increased psychopathological burden in the post-pandemic period highlights long-term mental health trajectories associated with the pandemic era. These emerging patterns of phenotypic complexity demonstrate that child and adolescent psychiatric services must transition from single-diagnosis models toward integrated care networks. Practically, strengthening community-based early intervention and creating rapid-access crisis support are essential to manage severe emotional dysregulation in the community and reduce acute psychiatric hospitalizations.

Background: Gastroesophageal reflux (GER) is common during infancy. Transient neuromotor features, including alteration in muscle tone, posture, and motor behaviour, have been observed in infants with GER symptoms. Methods: This retrospective observational study included 55 infants with clinical symptoms of GER, including 43 preterm and 12 term-born infants, evaluated at 3, 6, and 9 months (chronological or corrected age for preterms) using the Hammersmith Infant Neurological Examination (HINE). General Movements Assessment (GMA) and motor milestones were used as outcome indicators. Preterm cases were compared with 141 low-risk preterm controls. Linear Mixed-Effects Models (LMMs) with Bonferroni correction evaluated longitudinal Movements trajectories, while term-born infants were analyzed descriptively. Results: Global HINE scores progressively increased (3 months: 53.66 ± 5.75; 9 months: 68.35 ± 5.65), with no significant differences between preterm infants with GER symptoms and low-risk preterm controls. Conversely, the Movements subscale was consistently lower in the GER group at 3 (p = 0.001), 6 (p = 0.001), and 9 months (p < 0.001). LMM confirmed a significant association between GER symptoms and lower Movements scores (F = 47.405, p < 0.001; adjusted difference = −1.167), with a non-significant Group × Time interaction (p = 0.251), indicating no statistically significant evidence of different longitudinal trajectories. Bonferroni correction (α = 0.010) confirmed Movements as the only consistently reduced domain (p_adj < 0.005). Individual HINE items showed early discordance between axial and appendicular findings, followed by progressive neurological maturation. Conclusions: GER symptoms were associated with lower HINE Movements scores during the first 9 months, whereas standardized tone scores and global HINE profiles remained broadly comparable to low-risk controls. Subtle motor, tone, and postural findings observed during qualitative clinical examination should therefore be interpreted cautiously and within the broader neurological context, rather than considered in isolation. As an exploratory finding, GER symptoms may represent a relevant contextual factor when interpreting early neurological findings. Standardized examination tools like the HINE should be interpreted alongside qualitative clinical impressions and spontaneous movement quality during serial longitudinal assessments. These preliminary findings require confirmation in larger, prospective studies before their broader clinical implications can be established.