Prenatal exposure to alcohol (ethanol) in human and animal models results in a range of alcohol-induced developmental defects. In humans, those collective birth defects are called Fetal Alcohol Spectrum Disorders, with the most severe manifestation being Fetal Alcohol Syndrome (FAS). FAS is defined by pre- and post-natal growth retardation, minor facial abnormalities, and deficiencies in the central nervous system (CNS). The basal ganglia, one of the central nervous system components, are affected by exposure to ethanol during development. When exposed to alcohol in utero, the basal ganglia decrease in size resulting in poor motor coordination and defects in executive functioning.

Prenatal exposure to alcohol (ethanol) results in a continuum of physical, neurological, behavioral, and learning defects collectively grouped under the heading fetal alcohol spectrum disorders (FASD). Fetal alcohol syndrome (FAS) is the most severe combination of these defects under this heading, and is characterized by pre- and postnatal growth deficiencies, facial abnormalities, and defects of the central nervous system (CNS). The developing brain is particularly vulnerable to the toxicity of ethanol, given the broad time frame of susceptibility from neurulation, when the neural tube is formed, all the way through to birth. The cerebellum is an area of the brain particularly vulnerable to prenatal ethanol exposure. Mechanisms proposed for this drastic reduction in brain cells include apoptosis, oxidative stress, and damage to the radial glia stem cell progenitor pool. Physical dexterity, coordination, and visuospatial processing are all affected by these stressors, and eyeblink classical conditioning tests have proven that ethanol-induced damage goes beyond motor coordination by permanently impacting learning and memory.

Prenatal exposure to alcohol (ethanol) results in a continuum of physical, neurological, behavioral, and learning defects collectively grouped under the heading Fetal Alcohol Spectrum Disorder (FASD). Fetal Alcohol Syndrome (FAS) was first defined in 1973 as a condition characterized by pre- and postnatal growth deficiencies, facial abnormalities, and defects of the central nervous system. The pattern of facial defects that occur as a result of ethanol exposure during development primarily affects the midline of the face, altering morphology of the eyes, nose, and lips. Ethanol damage to cranial neural crest cells (CNCC) early in embryonic development is responsible for these minor midline abnormalities. Regulation of the gene sonic hedgehog (shh) during this period of development has been observed to rescue these ethanol-affected CNCC from fated cell death, an association that has not yet been examined as it applies to human cells.

Maternal consumption of alcohol (ethanol) during pregnancy can inhibit prenatal growth, resulting in fetuses that are small for gestational age. Those prenatal growth deficiencies can have lasting consequences for early childhood development and are often reflected by low weight and stature. Those alcohol-induced pre- and post-natal growth deficiencies ("failure to thrive") are among the abnormal developmental criteria used to identify Fetal Alcohol Syndrome (FAS). FAS is characterized by minor facial abnormalities and deficiencies of the central nervous system as well. A deficiency in prenatal growth is often referred to as an intrauterine growth restriction (IUGR), a general term that refers to stunted fetal growth that may be a result of genetic or environmental factors.