RESUMO
The first association between prenatal alcohol exposure and a teratogenic effect in the developing fetus was made in 1968 by pediatrician Paul Lemoine in France. A few years later, Jones and Smith defined the fetal alcohol syndrome which combined dysmorphic facial, growth and CNS features. The classic fetal alcohol syndrome has been recently reviewed. Current research is beginning to acknowledge that exposure to differing levels of prenatal alcohol cause a spectrum of clinical conditions which can be grouped under the umbrella term fetal alcohol spectrum disorder. There are three subtypes to fetal alcohol spectrum disorder: full fetal alcohol syndrome, partial fetal alcohol syndrome (where there is only partial facial dysmorphology) and alcohol-related neurodevelopmental disorder (where there is no facial dysmorphology and often absence of growth features). The term alcohol-related neurodevelopmental disorder is gradually replacing the older term fetal alcohol effects. These subtypes were initially described by Stratton and colleagues in 1996. It is also becoming clearer that the full fetal alcohol syndrome as originally described by Jones and Smith, and diagnosed in dysmorphic clinics, is the least common clinical subtype resulting from prenatal alcohol exposure. In addition, current and ongoing research on brain structure, shape and function indicates that the brain abnormality is not correlated with the facial dysmorphology or intelligence quotient. Therefore, the presence of full fetal alcohol syndrome does not necessarily mean that the patient has the most severe CNS impairments. Genetic research has suggested that genetic factors may have a role in a modulating a woman's susceptibility to having a baby with fetal alcohol spectrum disorder (specifically the full fetal alcohol syndrome subtype). Thus, genetic factors may increase the variability of the teratogenic effect of prenatal exposure to alcohol on the developing fetus.