STAMPA ANN. 07|06 - McGee

INTRODUCTION The teratogenic effects of alcohol on the developing brain have been known for over thirty years [1-3]. During this period, a host of neuropsychological and behavioral deficits associated with prenatal alcohol exposure have been identified and have helped to increase awareness of this public health concern. Although a limited number of autopsy studies have been competed, it was not until the utilization of imaging techniques during the last ten years that the opportunity to view the range of structural effects resulting from prenatal alcohol exposure on the living brain has been available. Perhaps the most widely recognized consequence of prenatal alcohol exposure is fetal alcohol syndrome (FAS). FAS is a major public health concern wherever women consume alcohol and the overall prevalence in the United States is estimated to be between 0.5 and 2.0 per 1000 births [4]. It is diagnosed based on a characteristic pattern of facial abnormalities, preand/or postnatal growth deficiency, and central nervous system (CNS) dysfunction. Facial alterations typically seen in individuals with FAS include short palpebral fissures, thin vermillion of the upper lip, and smooth philtrum. CNS dysfunction can be evidenced by functional and/or structural alterations depending on the specific diagnostic criteria used [5, 6]. Common functional impairments include deficits in overall intellectual ability, problem solving, language, social skills, and motor functioning. Structural alterations, the focus of this article, can be determined by brain imaging or at autopsy, or a proxy such as head circumference or neurological signs may be used. However, FAS is not the only consequence of prenatal alcohol exposure. Recently, the National Organization on Fetal Alcohol Syndrome coined the term fetal alcohol spectrum disorders (FASD) to describe the full range of effects resulting from prenatal exposure to alcohol. These effects range from FAS on the most severe end to subtle physical, cognitive, or behavioral effects. When considering the full range of effects, prevalence estimates of FASD are approximately 1 in 100 [7]. Various moderating factors have been proposed that may account for the variability of outcomes resulting from prenatal alcohol exposure. Some of these factors include genetic variation, timing and amount of alcohol consumed, nutrition, maternal age, socioeconomic status, and family and community resources [4]. FASD was not intended to be a diagnostic term, but serves to unify diagnostic labels such as Brain imaging and fetal alcohol spectrum disorders