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.

Sensory processing differences, reported in up to 97% of individuals with autism spectrum disorder (ASD), are increasingly recognized as a defining feature of the condition, shaping perception, cognition, and adaptive behavior. Atypical sensory responsivity, ranging from hyper- to hypo-reactivity and sensory seeking, emerges early in development and contributes to the clinical and neurobiological heterogeneity of autism. Alterations in neural connectivity, the balance of excitation and inhibition, and multisensory integration are thought to underlie these sensory profiles, influencing emotional regulation, attention, and social interaction. Sensory features also interact with co-occurring conditions such as anxiety, attention deficit hyperactivity disorder, and sleep and feeding difficulties, thereby shaping developmental trajectories and influencing adaptive behavior. Clinically, these sensory dysfunctions have a significant impact on daily participation and quality of life, extending their effects to family functioning. Understanding individual sensory phenotypes is therefore essential for accurate assessment and personalized intervention. Current therapeutic approaches include Sensory Integration Therapy, Sensory-Based Interventions, Sequential Oral Sensory Approach, and structured physical activity programs, often complemented by behavioral and mindfulness-based techniques. Emerging neuroplasticity-oriented methods for targeted modulation of sensory processing networks include neurofeedback and non-invasive brain stimulation. Overall, current evidence highlights the central role of sensory processing in ASD and underscores the need for multidisciplinary, individualized approaches to optimize developmental trajectories and enhance adaptive functioning. This review provides an updated synthesis of sensory processing in ASD, integrating neurobiological, developmental, and clinical evidence to highlight established knowledge, unresolved questions, and priorities for future research.

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.

Genetic dystonias are a heterogeneous group of movement disorders characterized by involuntary, sustained muscle contractions that cause repetitive movements and abnormal postures. Often beginning in childhood, they can significantly affect quality of life. Although individually rare, genetic causes are collectively relevant in pediatric dystonias, with over 250 associated genes. Among these, TOR1A, SGCE, and KMT2B are the most frequently reported in pediatric forms. Diagnosis is challenging due to the wide clinical and genetic variability. Recent advances in genetic testing, including whole-exome and whole-genome sequencing, have improved the early identification of causative variants. Functional data on selected mutations are helping to refine genotype–phenotype correlations. Management typically requires a multidisciplinary approach. Symptomatic treatments include anticholinergics, benzodiazepines, and botulinum toxin, while deep brain stimulation can be effective in refractory cases, especially in patients with TOR1A variants. Disease-modifying therapies are also emerging, such as gene therapy for AADC deficiency, highlighting the potential of precision medicine. This review provides an updated overview of pediatric genetic dystonias, with a focus on differential diagnosis and treatment strategies. Early and accurate diagnosis, together with personalized care, is key to improving outcomes in affected children.

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.