William Hunter’s Anatomia Uteri Humani Gravidi Tabulis Illustrata (The Anatomy of the Human Gravid Uterus Exhibited in Figures), hereafter called The Human Gravid Uterus, is an anatomical atlas depicting the pregnant form through both engravings and descriptions. William Hunter, an anatomist working in England during the eighteenth century, compiled the work based on observations from his dissections of pregnant women. The collection of thirty-four copper plate illustrations details the anatomy of the pregnant human womb (gravid uterus), and includes depictions of unborn fetuses at various stages of development. Hunter compiled The Human Gravid Uterus to provide an objective anatomical depiction of pregnancy and development at a time when midwifery and obstetrics were becoming prominent fields of medical practice in England.

Fetal surgeries are a range of medical interventions performed in utero on the developing fetus of a pregnant woman to treat a number of congenital abnormalities. The first documented fetal surgical procedure occurred in 1963 in Auckland, New Zealand when A. William Liley treated fetal hemolytic anemia, or Rh disease, with a blood transfusion. Three surgical techniques comprise many fetal surgeries: hysterotomy, or open abdominal surgery performed on the woman; fetoscopy, for which doctors use a fiber-optic endoscope to view and make repairs to abnormalities in the fetus; and percutaneous fetal theray, for which doctors use a catheter to drain excess fluid. As the sophistication of surgical and neonatal technology advanced in the late twentieth century, so too did the number of congenital disorders fetal surgeons treated, such as mylomeningeocele, blocked urinary tracts, twin-to-twin transfusion syndrome, polyhydramnios, diaphragmatic hernia, tracheal occlusion, and other anomalies. Many discuss the ethics of fetal surgery, as many consider it contentious, as fetal surgery risks both the developing fetus and the pregnant woman, and at times it only marginally improves patient outcomes. Some argue, however, that as more advanced diagnostic equipment and surgical methods improve, advanced clinical trials in a few conditions may demonstrate more benefits than risks to both pregnant women and fetuses.

The term Fetal Alcohol Syndrome (FAS) was first published in 1973 in an article published in the British medical journal The Lancet. In that article, a group of pediatricians and psychiatrists at the University of Washington Medical School helped to define the morphological defects and developmental delays that can affect children born to alcoholic mothers. Those observations include pre- and post-natal growth deficiencies, minor facial abnormalities, and damage to the developing brain that can result in behavioral, learning, and cognitive abnormalities.

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) is part of this group and was first defined in 1973 as a condition characterized by pre- and postnatal growth deficiencies, facial abnormalities and defects of the central nervous system (CNS). The CNS is particularly vulnerable to the effects of ethanol during prenatal development. Severe exposure correlates with gross morphological abnormalities and an overall decrease in white matter. Mechanisms for how ethanol affects the development of the CNS are complicated, but damage to neural stem cell progenitor pools that give rise to neurons and glia is strongly suspected to be a major factor. Damage to this population of cells at any point during CNS development can result in abnormalities in the formation and maturation of these cells, from the initial differentiation through the maturation of neuronal networks. This damage can lead to a wide variety of cognitive deficiencies, functional impairments, and behavioral problems depending on the area of the brain impacted by prenatal ethanol exposure.

Maternal consumption of alcohol (ethanol) can result 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 eye and ocular system development is particularly susceptible to the effects of prenatal alcohol exposure and can result in visual impairment or blindness.

Maternal consumption of alcohol (ethanol) during pregnancy can result in a continuum of embryonic developmental abnormalities that vary depending on the severity, duration, and frequency of exposure of ethanol during gestation. Alcohol is a teratogen, an environmental agent that impacts the normal development of an embryo or fetus. In addition to dose-related concerns, factors such as maternal genetics and metabolism and the timing of alcohol exposure during prenatal development also impact alcohol-related birth defects.

Prenatal exposure to alcohol (ethanol) can result in a continuum of developmental abnormalities that are highly variable depending on the severity, duration, frequency, and timing of exposure during gestation. Defects of the corpus callosum (CC) have proven to be a reliable indicator of prenatal alcohol exposure as it affects the brain. Structural abnormalities of the CC occur along a continuum, like most alcohol-induced anomalies, whereby more severe prenatal exposure results in a greater expression of the abnormal trait. A variety of cognitive deficiencies are associated with defects of the fetal CC, the morphology of which can vary greatly between individuals and can be observed through neuroimaging over a broad transect of life stages.

A variety of developmental defects occur as a result of prenatal exposure to alcohol (ethanol) in utero. In humans, those defects are collectively classified as Fetal Alcohol Spectrum Disorders, with Fetal Alcohol Syndrome (FAS) representing the more severe defects. FAS is defined by pre- and post-natal growth retardation, minor facial abnormalities, and deficiencies in the central nervous system (CNS). In addition to those defects, prenatal exposure to alcohol impacts cardiogenesis, the developmental stage of heart formation.

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.