Abstract

While the clinical syndrome characterized by prenatal alcohol abuse has been defined, the precise nature of central nervous system (CNS) deficits specifically associated with the duration and timing of alcohol exposure during pregnancy is less well defined. The majority of the fetal alcohol studies examining brain development has relied on animal model systems, particularly rodents, due to ethical and practical justifications. Earlier clinical findings indicated that women of different races were unequally at risk for delivering an FAS or ARBD baby following gestational alcohol abuse. The clinical evidence for fetal alcohol-induced neuropathology is sparse, mainly because most of the evidence comes from the few cases that have ended in autopsy. The discovery of facial dysmorphology in animal models for the study of FAS came from experiments performed on mice, nonhuman primates, and beagles. Numerous experimental studies have found that alcohol exposure during the third trimester equivalent produces microencephaly, even when somatic growth retardation occurs.

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