Children exposed to substantial amounts of alcohol prenatally are known to display a range of physical and cognitive anomalies, referred to as fetal alcohol spectrum disorders (FASDs).
Animal models and neuroimaging studies of FASDs have consistently demonstrated that specific regions of the brain (e.g., midline structures) are more vulnerable to the teratogenic effects of alcohol than other regions.
The main aim of this article is to assess whether findings from cognitive–behavioral studies of FASDs yield a profile that maps onto the pattern of damage revealed by neuroanatomical investigations.
To achieve this aim, the findings from studies that have investigated elementary functions (e.g., associative learning), general functions (e.g., intellectual abilities), specific functions (e.g., language and memory) and behavior in children and adults with FASDs are examined.
The cognitive–behavioral profile emerging from the data is defined as a generalized deficit in processing and integrating complex information. It is proposed that slow processing of information mainly contributes to this deficit.
The clinical implications of the above characterization of the cognitive–behavioral profile in FASDs are discussed.
