No abstract

In this scoping review, we examined the association between maternal nutrition during pregnancy and neurodevelopment in offspring. We searched the Pubmed and ScienceDirect databases for articles published from 2000 to 2020 on inadequate intake of vitamins (B12, folate, vitamin D, vitamin A, vitamin E, vitamin K), micronutrients (cooper, iron, creatine, choline, zinc, iodine), macronutrients (fatty acids, proteins), high fat diets, ketogenic diets, hypercaloric diets, and maternal undernutrition. Some older relevant articles were included. The search produced a total of 3590 articles, and 84 studies were included in the qualitative synthesis. Data were extracted and analyzed using charts and the frequency of terms used. We concluded that inadequate nutrient intake during pregnancy was associated with brain defects (diminished cerebral volume, spina bifida, alteration of hypothalamic and hippocampal pathways), an increased risk of abnormal behavior, neuropsychiatric disorders (ASD, ADHD, schizophrenia, anxiety, depression), altered cognition, visual impairment, and motor deficits. Future studies should establish and quantify the benefits of maternal nutrition during pregnancy on neurodevelopment and recommend adequate supplementation.

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Animal-assisted therapy may be useful as a complementary intervention in the management of children with CP and pain. Although results are in general positive for the management of children with Down syndrome and autism, the diversity of scales used to measure outcomes makes it difficult to establish true effectiveness. The application of simple corrective measures in the randomization process would greatly improve the quality of evidence. It is necessary to reach a consensus between AAT researchers regarding appropriate instruments to provide higher-quality evidence in further studies.

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EF measures in children with ADHD revealed more problems, particularly those having to do within planning, inhibition, working memory and cognitive control. Age and sex may affect the degree of EF impairment.

Background: Undiagnosed children with neurodevelopment delay disorders (NDD) frequently experience school difficulties, leading to school desertion or academic failure with subsequent familial, social and work-related problems. Methods: In 2004–2005, we conducted a cross-sectional study to determine the prevalence of developmental delay among preschoolers in Bogotá (Colombia); convenience samples in several socioeconomic areas of the city were screened to define the prevalence of NDD. Parents and teachers were interviewed to identify children with possible NDD. Selected children were evaluated with a neurodevelopmental abbreviated scale (EAD-1). Results: We screened 2,043 preschool children aged <60 months; 288 suspected cases were examined individually using the EAD-1 scale. One or more abnormal items (alert category) were found in 67 (23.3%) children, for an estimated prevalence of 32.8‰ children <5 years of age, including deficits in gross motor function (9.3‰), personal-social interactions (9.8‰), fine motor skills (10.3‰), auditory language delay (18.6‰) and overall delay (10.8‰). Conclusions: There is limited information regarding the prevalence of neurodevelopmental delay in nonindustrialized countries. The prevalence obtained in Bogotá, Colombia, is within the expected range; however, we identified NDD among apparently healthy children from nurseries and kindergartens, who had previously been undiagnosed and untreated. Lack of evaluation of developmental milestones in children in Colombia is a substantial public health problem that will require effective intervention.

Attention deficit hyperactivity disorder (ADHD) is one of the most highly heritable behavioral disorders in childhood, with heritability estimates between 60 and 90 %. Family, twin and adoption studies have indicated a strong genetic component in the susceptibility to ADHD. The synaptosomal-associated protein of molecular weight 25 kDa (SNAP25) is a plasma membrane protein known to be involved in synaptic and neural plasticity. Animal model studies have shown that SNAP25 gene is responsible for hyperkinetic behavior in the coloboma mouse. In recent studies, several authors reported an association between SNAP25 and ADHD. In this study, we used a case-control approach to analyze the possible association of two polymorphisms of SNAP25 for possible association with ADHD in a sample of 73 cases and 152 controls in a Colombian children population. Polymorphisms are located in 3' untranslated region of SNAP25, positions T1065G and T1069C. We found a significant association with the GT haplotype (rs3746554|rs1051312) of SNAP25 (p = 0.001). Evidence of association was also found for the G/G genotype of rs3746554 (p = 0.002) and C/C genotype of rs1051312 (p = 0.009). This is the first study in a Latin American population. Similar to other studies, we found evidence of the association of SNAP25 and ADHD.