Fetal alcohol syndrome

Abstract

Maternal alcohol consumption during pregnancy is known to produce a spectrum of morphological and neurocognitive outcomes in the offspring. The most severely affected on the spectrum exhibit a cluster of birth defects called fetal alcohol syndrome, which is characterized by a unique pattern of anomalies on the face, prenatal and/or postnatal growth deficiency, and evidence of central nervous system (CNS) dysfunction (Jones et al. 1973). The characteristic pattern of malformations on the face includes a smooth philtrum, thin upper lip, and short palpebral fissures (see Fig. 80.1). Children with FASD are usually small in stature, with their height and weight falling below the 10th percentile. The deleterious effects of alcohol on the central nervous system are evidenced by microcephaly and cognitive and behavioral deficits. Children with prenatal alcohol exposure have also been observed to exhibit birth defects involving other systems such as cardiac (e.g., atrial and ventricular septal defects), skeletal (e.g., clinodactyly and camptodactyly), ocular (e.g., strabismus), and auditory (e.g., conductive hearing loss). However, the majority of children on the spectrum display only some or none of the above physical features but exhibit evidence of CNS dysfunction. The term, alcohol-related neurodevelopmental disorder (ARND), is used to label neurodevelopmental difficulties in those alcohol-exposed children without clinically discernable physical anomalies (Stratton et al. 1996). Although not a diagnostic label, the term fetal alcohol spectrum disorders (FASDs) has been introduced to denote the full spectrum of morphological and neurocognitive outcomes resulting from prenatal alcohol exposure. While estimated prevalence rates of FAS range from.5 to 2 cases per 1,000 live births, the rate of FASD is estimated at 1 per 100 (Sampson et al. 1997)