Background and Objectives: Late preterm (LP) infants (born between 34 and 36 weeks of gestational age) are considered at higher risk of neonatal morbidities, mortality, and neurological impairments than full-term born infants (FT). The aim of this study was to provide a critical review of the literature outlining the different aspects of neurological function reported both in the neonatal period and in the follow up of late preterm infants. Materials and Methods: A comprehensive search of the MEDLINE, Embase, PsycINFO, and CINAHL electronic databases was made, using the following search terms: ‘Late preterm infants’, ‘Near term infants’, ‘neurological assessment’, ‘neurological outcome’, ‘neuromotor outcome’, cerebral palsy’, ‘CP’, ‘motor impairment’, including all the studies reporting clinical neurological assessment of LP (including both neonatal period and subsequent ages). Results: A total of 35 articles, comprising 301,495 children, were included as fulfilling the inclusion criteria: ten reported neonatal neurological findings, seven reported data about the first two years after birth, eighteen reported data about incidence of CP and motor disorder during the infancy. Results showed a more immature neurological profile, explored with structured neurological assessments, in LP infants compared with FT infants. The LP population also had a higher risk of developing cerebral palsy, motor delay, and coordination disorder. Conclusion: LP had a higher risk of neurological impairments than FT infants, due to a brain immaturity and an increased vulnerability to injury, as the last weeks of gestational age are crucial for the development of the brain.

Objective: Highly purified cannabidiol (CBD) is approved as adjunctive therapy for seizures associated with Dravet syndrome (DS), Lennox–Gastaut syndrome (LGS), and tuberous sclerosis complex (TSC), although its role in other developmental and epileptic encephalopathies (DEEs) remains unexplored. The aim of this study was to assess the real‐world use, efficacy, and safety of CBD across a broad cohort of patients with DEEs, including off‐label indications. Methods: In this retrospective study, we evaluated 107 patients with DEEs treated with CBD for ≥3 months between 2020 and 2024. Data on seizure frequency, tolerability, retention, and non‐seizure outcomes were collected. Efficacy was defined as ≥50% or ≥75% seizure reduction. Statistical analyses explored predictors of response. Results: Patients had LGS (55.1%), DS (16.8%), TSC (8.4%), or other DEEs (19.6%), with a genetic etiology in 56.1%. At a median follow‐up of 20 months, 69% achieved ≥50% seizure reduction, and 21% achieved ≥75% reduction. Patients with LGS, TSC, and other DEEs showed higher efficacy and retention rates compared to DS. Genetic or unknown etiology was associated with better outcomes ( p = 0.011). Combination with valproate was associated with reduced efficacy ( p = 0.006), while combination with clobazam had no significant effect on efficacy nor safety. Non‐seizure improvements included increased alertness (56%), improved sleep quality (25%), and enhanced motor performance (14%). Adverse events occurred in 33.6%, mostly mild and transient; 9% discontinued due to side effects. Significances: This study confirms the effectiveness and good tolerability of CBD in a real‐world DEE population, including off‐label use. These findings support expanding CBD indications and underscore the need for prospective studies targeting both seizure and developmental outcomes. Plain language summary: This study looked at the use of cannabidiol (CBD), a cannabis‐based medicine, in 107 people with severe forms of epilepsy called developmental and epileptic encephalopathies (DEEs). With CBD add‐on, about two‐thirds of patients had fewer seizures, and some caregivers noticed improvements in alertness, sleep, or movement. Most patients tolerated the treatment well, but some experienced side effects, and a few had to stop taking it. While the results are promising, more research is needed to confirm how effective and safe CBD is for different types of DEEs, especially those not currently approved for treatment with CBD.

Background/Objectives: Autism spectrum disorder (ASD) has been extensively studied through neuroimaging, primarily focusing on grey matter and more in children than in adults. Studies in children and adolescents fail to capture changes that may dampen with age, thus leaving only changes specific to ASD. While grey matter has been the primary focus, white matter (WM) may be more specific in identifying the particular biological signature of the neurodiversity of ASD. Diffusion tensor imaging (DTI) is the more appropriate tool to investigate WM in ASD. Despite being introduced in 1994, its application to ASD research began in 2001. Studies employing DTI identify altered fractional anisotropy (FA), mean diffusivity, and radial diffusivity (RD) in individuals with ASD compared to typically developing (TD) individuals. Methods: We systematically reviewed literature on 21 May 2025 on PubMed using the following strategy: (“autism spectrum”[ti] OR autistic[ti] OR ASD[ti] OR “high-functioning autism” OR Asperger*[ti] OR Rett*[ti]) AND (DTI[ti] OR “diffusion tensor”[ti] OR multimodal[ti] OR “white matter”[ti] OR tractograph*[ti]). Our search yielded 239 results, of which 26 were adult human studies and eligible. Results: Analysing the evidence, we obtained regionally diverse WM alterations in adult ASD, specifically in FA, MD, RD, axial diffusivity and kurtosis, neurite density, and orientation dispersion index, compared to TD individuals, mostly in frontal and interhemispheric tracts, association fibres, and subcortical projection pathways. These alterations were less prominent than those of children and adolescents, indicating that individuals with ASD may improve during brain maturation. Conclusions: Our findings suggest that white matter alterations in adults with ASD are regionally diverse but generally less pronounced than in younger populations. This may indicate a potential improvement or adaptation of brain structure during maturation. Further research is needed to clarify the neurobiological mechanisms underlying these changes and their implications for clinical outcomes.

Objective: Lennox–Gastaut syndrome (LGS) is a developmental and epileptic encephalopathy defined by polymorphic seizures, intellectual disability (ID), and characteristic electroencephalographic (EEG) patterns. The applicability and biological validity of current electroclinical criteria remain debated. This study evaluated the concordance between clinical and electroclinical definitions of LGS and applied unsupervised clustering to identify data‐driven profiles within LGS. Methods: We retrospectively analyzed patients clinically fulfilling LGS criteria, with longitudinal electroclinical documentation and at least one sleep EEG. Patients meeting complete electroclinical criteria were compared with those meeting clinical criteria alone. Additionally, exploratory unsupervised K‐modes clustering and discriminant correspondence analysis were applied in adolescent and adult patients. Results: We included 105 patients (60.9% female), with a median age of 24 years (interquartile range = 16–35). Sixty‐nine patients (65.7%) met complete electroclinical criteria, yet neurodevelopmental features, seizure types, magnetic resonance imaging (MRI) findings, and treatment refractoriness were comparable to the clinically defined subgroup. K‐modes clustering ( n = 97 patients) identified three data‐driven electroclinical profiles. Cluster 1 comprised patients with the earliest seizure onset, profound intellectual and motor impairment, EEG background slowing, lower prevalence of generalized paroxysmal fast activity (GPFA), highest prevalence of structural etiologies, and lowest likelihood of meeting complete electroclinical criteria for LGS. Among clusters more frequently fulfilling complete electroclinical criteria, Cluster 2 represented an early onset profile with higher rates of ID, EEG background slowing, and high prevalence of polymorphic seizures. Cluster 3 included comparatively preserved patients, characterized by later onset, milder neurodevelopmental impairment, and higher frequency of normal MRI. Despite similar clinical severity, Cluster 1 patients had undergone fewer antiseizure medication trials. Significance: Exploratory data‐driven clustering identified clinically relevant electroclinical profiles that may help refine phenotypic stratification within clinically defined LGS. These included a severe GPFA‐underrepresented profile and two GPFA‐positive phenotypes differing in developmental severity, seizure profile, and age at onset.

Objective: CDKL5 deficiency disorder (CDD) is an early‐onset developmental and epileptic encephalopathy characterized by frequent drug‐resistant seizures, cerebral visual impairment, motor dysfunction, and sleep and gastrointestinal disturbances. Preliminary evidence suggests that highly purified cannabidiol (CBD) may reduce seizure frequency, but data on its effects on comorbidities are lacking. This study aimed to evaluate the efficacy and safety of CBD in individuals with CDD. Methods: We conducted a prospective, open‐label, single‐center study including patients with CDD aged >1 year. Outcomes included motor seizure frequency, caregiver‐ and clinician‐rated Clinical Global Impression (CGI), and changes in sleep, motor abilities, and EEG at 3, 6, and 12 months. CBD plasma levels were measured with High‐Performance Liquid chromatography–Mass Spectrometry (HPLC‐MS). Results: Eight of nine patients (all females; median age 10 years, range 1–24) completed the study, with a retention rate at 12 months of 8/9 (89%). One discontinued at 6 months due to a skin rash. A > 50% seizure reduction was observed in 8/9 patients at 3 months, 6/9 at 6 months, and 1/8 at 12 months. Seven patients showed some degree of vigilance improvements, three in motor performance, and two in sleep and constipation. All caregivers reported at least minimal overall improvement (CGI score 3) at 3 months, and three reported marked improvement (CGI score 2), with a peak at 3 months. Five patients showed adverse events during the trial, but none were considered serious. The median CBD dose at all time‐points was 15.6 mg/kg/day (IQR 10.0–18.9) corresponding to a plasma dose of 69.9 ng/mL (IQR 29.8–114.6) and the median concentration/dose ratio was 4.7 (IQR 2.7–6.8). Significance: The safety and efficacy of highly purified CBD in CDD were consistent with previous reports in the literature, with possible benefits beyond seizure control. Further studies are warranted to assess non‐seizure outcomes and compare long‐term efficacy across treatment options. Plain Language Summary: We studied nine girls with CDKL5 deficiency disorder who had frequent, hard‐to‐treat seizures. They received cannabidiol for up to 1 year, added to their usual medicines. Most children had fewer seizures in the first months of treatment. Some families also noticed better alertness, eye contact, movement, sleep, or constipation. Side effects were usually mild and manageable. Although seizure frequency often returned to baseline by the end of the study, most families chose to continue cannabidiol. Because this was a small study without a placebo group, these results are preliminary, and larger controlled trials are needed.