Fetal alcohol syndrome (FAS) is caused by maternal consumption of alcohol during pregnancy, though it is not clear how much alcohol is required to result in the syndrome. Children with FAS exhibit a wide range of symptoms such as severe growth restriction, facial dysmorphology (i.e., smooth philturm, thin upper lip, small palpebral fissures), and intellectual disability. It affects 0.2 to 1.5 individuals per 1000 births across various populations and is at comparable or increased rates relative to other neurodevelopmental disorders such as Down syndrome. The relatively high incidence of FAS in the US is of considerable social concern given that it is a leading cause of preventable developmental disabilities (1). Further, children with all required features to obtain a diagnosis of FAS are not the only ones negatively affected; those with severe prenatal alcohol exposure, but without facial dysmorphology required for the FAS diagnosis have also exhibited neurocognitive deficits (2) and brain abnormalities (3,4). The brain is particularly vulnerable to the teratogenic effects of prenatal alcohol exposure. Microcephaly was among the first noted gross neural abnormalities in children born to alcohol abusing mothers (5) and has been consistently confirmed in postmortem and in vivo studies (6).

The paper by Maluszic and colleagues (7) used structural and functional MRI (fMRI), finding differences in brain activation during working memory (WM) tasks in children and adults with fetal alcohol spectrum disorders (FASD) including FAS, partial FAS, and alcohol related neurodevelopmental disorder (ARND). The maintenance of structural brain changes into adulthood described above raises the specter of potentially permanent functional changes following prenatal exposure to alcohol. Although the study is preliminary, it is the first published study thus far to examine brain function in FASD using fMRI, and hopefully will encourage further study into this disorder using advanced imaging methods.

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