Acute Disseminated Encephalomyelitis followed by Optic Neuritis: A Rare Syndrome of Uncertain Treatment and Prognosis

Aim Acute Disseminated Encephalomyelitis followed by optic neuritis (ADEM-ON), first described in 2013, is a rare demyelinating syndrome, typical of the pediatric age. We conducted a mini review of the existing literature, focusing on clinical, laboratory, radiological, therapeutic, and prognostic aspects in order to improve the identification of new cases. Methods We searched PubMed and Cochrane Library for studies on ADEM-ON between 2013 and 2018. Results Examination of the reported cases (three case reports and eight observational studies) established the following features. Time between ADEM and ON is highly variable. Almost all patients show antimyelin oligodendrocyte glycoprotein antibody (MOG-abs) seropositivity. High-dose intravenous steroid and plasmapheresis efficacy is reported for the acute phase; oral prednisone and other maintenance drugs may be useful in avoiding relapses. The clinical history may lead to a complete recovery but also to residual deficits. Conclusion MOG-abs detection strongly supports ADEM-ON diagnosis, confirming this entity as part of MOG-abs spectrum disorder. Owing to the very small number of cases so far reported, predicting clinical evolution is very difficult

Vitamin D Deficiency in Autism Spectrum Disorder: A Cross-Sectional Study

Vitamin D plays a role in central nervous system (CNS) development. Recent literature focused on Vitamin D status in children and adolescents with autism spectrum disorder (ASD), but with inconsistent results. Our case-control study is aimed at evaluating serum 25-hydroxyl-Vitamin D (25(OH)D) concentration in children with ASD (ASD group, n=54) compared to children affected by other neurological and psychiatric disorders (non-ASD group, n=36). All patients were admitted at the Complex Operative Unit of Child Neuropsychiatry, Polyclinic of Bari, Italy. 25(OH)D was quantified by chemiluminescence immunoassay and level defined as: Deficiency (<20 ng/mL); insufficiency (20-30); normality (30-100); toxicity (>100). Statistical analysis was performed using SPSS20 (significance<0.05). The ASD group showed 25(OH)D a mean level significantly lower than control (p=0.014). Multivariable logistic regression analysis showed an association between ASD and Vitamin D deficiency (p=0.006). The nature of such association is unclear. Vitamin D deficiency may probably act as a risk factor for the development of ASD. Further studies are needed to unravel the role of Vitamin D in ASD etiology and investigate its therapeutic potential

Nutraceuticals and their role in tumor angiogenesis

Angiogenesis plays a pivotal role in cancer initiation, maintenance, and progression. Diet may inhibit, retard or reverse these processes affecting angiogenesis (angioprevention). Nutraceuticals, such as omega-3 fatty acids, amino acids, proteins, vitamins, minerals, fibers, and phenolic compounds, improve health benefits as they are a source of bioactive compounds that, among other effects, can regulate angiogenesis. The literature concerning the pro-angiogenic and/or anti-angiogenic nutraceuticals and the possible activated pathways in cancer and other non-neoplastic diseases by in vivo and in vitro experiments are reviewed

Eating and mealtime behaviors in patients with autism spectrum disorder: Current perspectives

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impaired social and communication skills and repetitive and restrictive behaviors. Children and adolescents with ASD are more likely to present feeding problems than their typically developing peers are. The present narrative review of literature aims to highlight the most recent evidence about epidemiology and presentations of eating and mealtime behavioral abnormalities in ASD from infancy to adolescence. Abnormalities in breastfeeding and acceptance of complementary foods have been described by most of the studies evaluating ASD early feeding history. Among the various eating and mealtime behaviors identified in ASD children and adolescents, the most common was food selectivity. The present review also provides brief overviews of the various aspects of food that may influence food acceptance by ASD patients and of the correlation between eating problems and ASD core symptoms, as well as with cognitive level, language skills, and family environment. However, studies evaluating eating problems in ASD children and adolescents are very heterogeneous and they show methodological differences. Moreover, the absence of unique definitions of eating and mealtime behaviors in ASD further limits the comparability of studies

Coupled ocean-land millennial-scale changes 1.26 million years ago, recorded at Site U1385 off Portugal

While a growing body of evidence indicates that North Atlantic millennial-scale climate variability extends to the Early Pleistocene, its impact on terrestrial ecosystems has not been established. Here we present ultra-high resolution (70–140 year) joint foraminiferal isotopic and pollen analyses from IODP Site U1385 off Portugal, focusing on a short glacial section of Marine Isotope Stage 38, ~ 1.26 million years ago. Our records reveal the presence of millennial-scale variability in the coupled ocean–atmosphere–land system in the North Atlantic and provide the first direct evidence for the response of western Iberian vegetation to abrupt climate changes in the Early Pleistocene. The magnitude and pacing of changes bear significant similarities to Dansgaard–Oeschger variability of the last two glacials

Traumatic experiences in childhood and adolescence: a meta-analysis of prospective studies assessing risk for psychosis

Evidence of the association between traumatic experiences and psychosis are uncertain with respect to temporal order, clinical outcomes and the role of the age and genetic liability. The aim of the present meta-analysis was to explore the temporal relationship between the development of psychosis and traumatic exposure using prospective studies and to examine the role of moderation factors on overall effect sizes. Studies were identified by searching Embase-Ovid, PsycINFO (EBSCO), Pubmed, Scopus, Web of Science databases, and yielded an initial total of 9016 papers, leaving finally 23 after the screening process. Three sets of meta-analyses estimated the risk of developing psychotic experiences or full clinical psychosis by having experienced maltreatment by an adult or bullying by peers or parental death, using the random-effects model. Bullying by peers (OR = 2.28 [1.64, 4.34]), maltreatment by an adult (OR = 2.20 [1.72, 2.81]) and parental death (OR = 1.24 [1.06, 1.44]) all increased the risk of psychosis. Moderator analysis showed that negative effects of bullying were detected especially in those with genetic liability for psychosis and exposure to multiple trauma types; studies with higher prevalence of males showed a stronger risk for those exposed to parental death. No significant meta-regression was found between the risk of developing a full clinical psychosis or a psychotic experience. Lack of studies hampered the results about the age of trauma occurrence. The cumulative effect of being bullied from peers and experiencing other adversities during childhood and/or adolescence, together with genetic liability for psychosis, appears to confer the highest risk for developing psychotic symptoms later in life

DRD1 and DRD2 Receptor Polymorphisms: Genetic Neuromodulation of the Dopaminergic System as a Risk Factor for ASD, ADHD and ASD/ADHD Overlap

The dopaminergic system (DS) is one of the most important neuromodulator systems involved in complex functions that are compromised in both autism spectrum disorder (ASD) and attention deficit/hyperactivity disorder (ADHD), conditions that frequently occur in overlap. This evidence suggests that both disorders might have common neurobiological pathways involving the DS. Therefore, the aim of this study was to examine the DRD1 and DRD2 dopamine receptor single nucleotide polymorphisms (SNPs) as potential risk factors for ASD, ADHD, and ASD/ADHD overlap. Genetic data were obtained from four groups: 75 ASD patients, 75 ADHD patients, 30 patients with ASD/ADHD overlap, and 75 healthy controls. All participants were between 2 and 17 years old. We compared the genotypic and allelic frequency of 18 SNPs among all of the study groups. Moreover, in the case of statistically significant differences, odds ratios (OR) were obtained to evaluate if the presence of SNPs might be a risk factor of developing a specific clinical phenotype. This study found that DRD1 and DRD2 receptors SNPs might be considered as potential risk factors for ASD and ADHD. However, only DRD2-12 (rs7131465) was significantly associated with a higher risk for the ASD/ADHD overlap. These data support the hypothesis of the genetic neuromodulation of the DS in the neurobiology of these conditions

14q12q13.2 microdeletion syndrome: Clinical characterization of a new patient, review of the literature, and further evidence of a candidate region for CNS anomalies

Background: Chromosome 14q11-q22 deletion syndrome (OMIM 613457) is a rare contiguous gene syndrome. Two regions of overlap (RO) of the 14q12q21.1 deletion have been identified: a proximal region (RO1), including FOXG1(*164874), NKX2-1(*600635), and PAX9(*167416) and a distal region (RO2), including NKX2-1 and PAX9. We report a 6-year-old boy with mild dysmorphic facial features, global developmental delay, and hypoplasia of the corpus callosum. Methods and Results: Array-CGH analysis revealed a 14q12q13.2 microdeletion. We compared the phenotype of our patient with previously published cases in order to establish a genotype–phenotype correlation. Conclusion: The study hypothesizes the presence of a new RO, not including the previously reported candidate genes, and attempt to define the associated molecular and psychomotor/neurobehavioral phenotype. This region encompasses the distal breakpoint of RO1 and the proximal breakpoint of RO2, and seems to be associated with intellectual disability (ID), hypotonia, epilepsy, and corpus callosum abnormalities. Although more cases are needed, we speculated on SNX6(*606098) and BAZ1A(*605680) as potential candidate genes associated with the corpus callosum abnormalities