Alcohol intake by women before planning a pregnancy, during pregnancy, and/or during lactation induces brain, behavioral, and physical abnormalities in the fetus, which are known as fetal alcohol spectrum disorders. Thanks to the availability of animal models, some cellular and biochemical processes affecting offspring exposed to ethanol during early development have been extensively investigated. Ethanol effects may be mitigated or increased if offspring also are exposed to either positive or adverse conditions during early life. These environmental conditions may have an impact on neuronal and behavioral development and may increase the risk of developing neuropsychiatric symptoms. Indeed, brain development largely is modifiable by experiences, and neuroplasticity is particularly evident during early phases of life. Molecular mediators for brain development and synaptic plasticity are neurotrophins, such as nerve growth factor and brain-derived neurotrophic factor. Early ethanol exposure not only affects the fetal brain directly, but it also leads to long-lasting consequences that emerge during adulthood and aging. Although the mechanisms responsible for these abnormalities in the fetus are unclear, it is hypothesized that ethanol might damage the central nervous system through oxidative stress processes by increasing free-radical production and decreasing cellular antioxidant ability. Ethanol’s effects on animal models have been investigated in detail; however, only few studies have investigated the consequences of early wine consumption. Wine contains several concentrations of ethanol and is consumed largely by Mediterranean populations. We recently compared the consequences of early exposure to ethanol or red wine (at the same ethanol concentration) administered during different stages of development in animal models. Our studies show a series of behavioral and neurologic abnormalities in juvenile, adult, and aged offspring of mice exposed to ethanol. A much smaller number of changes (if any) were evidenced as a consequence of early exposure to red wine. Antioxidant compounds measurable in red wine may have mitigated the toxicity associated with ethanol in the fetus. These “protective” mechanisms in mice pre- and postnatally exposed to red wine, compared with the ethanol group, remain unknown. As a whole, our data should not be interpreted as encouraging women to consume red wine before or during pregnancy and/or lactation. Indeed, in these cases, alcohol intake absolutely must be avoided.

The last two decades have witnessed a rapid growth of published data on the cognitive and behavioral functioning of children with fetal alcohol spectrum disorders (FASD). The main of aim of this paper is to review cognitive and behavioral data on FASD using a causal modeling framework originally proposed by Morton and Frith [1, 2], according to which data pertinent to a neurodevelopmental disorder can be organized at three levels: neurobiology, cognition, and behavior. In this review, we confine ourselves to reviewing the studies of cognitive abilities and behavior in children with FASD. The studies of cognitive functions can be further divided into two groups: those of elementary functions (e.g., reflexive orienting responses) and those of complex functions (e.g., language, memory). There is evidence that children with FASD are slower at reflective orienting responses and exhibit deficits in associative learning. The pattern of results emerging from the studies of complex cognitive functions is that the FASD group shows performance decrements with increased task complexity. At the behavioral level, children with prenatal alcohol exposure are rated as showing deficient adaptive skills, particularly in the social domain. These children have also been observed to show deficits in executive functioning with notable behavioral and emotional regulatory problems. A broad range of risk factors including the alcohol’s teratogenicity seem to interactively contribute to these cognitive and behavioral problems.

Children with developmental coordination disorder (DCD) are characterized by participation restrictions. Participation, a central concept in the International Classification of Functioning, Disability and Health - Children and Youth Version (ICF-CY; WHO, 2007), is a dynamic process that occurs between individuals and their environment. The aim of this review is to emphasize the role of early identification of children with DCD as an important factor in predicting their participation in daily life. This review discusses issues such as by whom and how this early identification is achieved, at what point within the developmental sequence and in which contexts, and the parents’ role to this process and contribution to their children’s participation. Finally, future directions for advancing research and practice towards enhancing the participation of children with DCD are discussed in relation to the children's attendance, belonging and involvement in varied life domains.

Attention deficit hyperactivity disorder (ADHD) is not only highly prevalent, persistent and impairing but also is one of the most heritable of all psychiatric disorders. As a result, ADHD has been the focus of considerable genetic research. The results of recent genetic studies are reviewed with a focus on the emerging picture and future trends. ADHD appears to be a complex disorder in which multiple genetic and environmental risks contribute to a quantitative trait. At the same time, there is growing evidence that in a proportion of cases, individually rare variants such as copy number variants may play an important causal role. The more genetic risks, both common and rare, the more extreme the trait. With increasing samples and advanced genetic methods, single nucleotide polymorphism (SNPs) and copy number variants (CNVs) conferring risk for ADHD are being identified. Further study will be required before we can understand the causal significance of these findings. Increased sample size is an urgent necessity if we are to discover potentially causal variants. Non-behavioral markers of genetic risk known as endophenotypes could also play a role in parsing the phenotypic and genetic heterogeneity of ADHD as they have in other complex disorders. Genetic studies in ADHD hold the potential for refined nosology, more precise diagnosis, and differential diagnosis, improved early identification leading to novel intervention strategies and identification of innovative targets for therapeutics based on a precise understanding of disease mechanism.

Autism spectrum disorder (ASD) is a behaviorally defined neurodevelopmental disorder associated with the presence of social-communication deficits and restricted and repetitive behaviors. In the latest conceptualization of ASD, these two behavioral dimensions represent the core defining features of ASD, whereas associated dimensions, such as intellectual and language ability, provide a means for describing the ASD heterogeneity. In addition, the characterization of ASD subgroups, defined by the presence of known medical, genetic, or other psychiatric disorders, furthers our understanding of ASD heterogeneity. This paper reviews the history of autism, describes its core defining features, and provides an overview of the clinically and etiologically relevant subgroups that add to the complexity of this condition.