Fetal alcohol syndrome is a devastating developmental disorder caused by prenatal exposure to high amounts of alcohol. In addition to structural abnormalities and growth deficits, fetal alcohol syndrome is associated with a broad spectrum of neurobehavioral anomalies. This paper reviews the behavioral and cognitive effects of prenatal alcohol exposure. More than 20 years of research are discussed, with a focus on IQ, activity, attention, learning, memory, language, motor, and visuospatial abilities in children prenatally exposed to varying amounts of alcohol, including those with fetal alcohol syndrome.

A Review of the Neurobehavioral Deficits in Children with Fetal Alcohol Syndrome or Prenatal Exposure to Alcohol

In biomedical scientific investigations, expositions of findings are conceptually simplest when they comprise comparisons of discrete groups of individuals or involve discrete features or characteristics of individuals. But the descriptive benefits of categorization become outweighed by their limitations in studies involving dose-response relationships, as in many teratogenic and environmental exposure studies. This article addresses a pair of categorization issues concerning the effects of prenatal alcohol exposure that have important public health consequences: the labeling of individuals as fetal alcohol syndrome (FAS) versus fetal alcohol effects (FAE) or alcohol-related neurodevelopmental disorder (ARND), and the categorization of prenatal exposure dose by thresholds. We present data showing that patients with FAS and others with FAE do not have meaningfully different behavioral performance, standardized scores of IQ, arithmetic and adaptive behavior, or secondary disabilities. Similarly overlapping distributions on measures of executive functioning offer a basis for identifying alcohol-affected individuals in a manner that does not simply reflect IQ deficits. At the other end of the teratological continuum, we turn to the reporting of threshold effects in dose-response relationships. Here we illustrate the importance of multivariate analyses using data from the Seattle, Washington, longitudinal prospective study on alcohol and pregnancy. Relationships between many neurobehavioral outcomes and measures of prenatal alcohol exposure are monotone without threshold down to the lowest nonzero levels of exposure, a finding consistent with reports from animal studies. In sum, alcohol effects on the developing human brain appear to be a continuum without threshold when dose and behavioral effects are quantified appropriately.

On categorizations in analyses of alcohol teratogenesis.

Behavioral teratology of alcohol.

In the 20 years since fetal alcohol syndrome (FAS) was identified as a birth defect, relatively few studies have described adolescents and adults with this disability, although FAS is thought to be the leading known cause of mental retardation. Many practical problems exist in accruing a population of adolescent and adult patients with FAS and in following them systematically past childhood. Yet by examining the natural history of FAS, it should be possible to evaluate the long-term needs of these patients and to develop an appropriate set of lifetime interventions suitable to their disabilities. Taking a historical perspective, this article reviews the pertinent literature, describing the findings of several long-term follow-up studies of children with FAS. It raises questions about the needs of adolescents and adults with FAS that should be addressed through future research and public policy. FAS: THE INITIAL RESEARCH FAS is growing up. It is now 20 years since Jones and Smith (1973) coined the term "fetal alcohol syndrome" to describe children who had a specific and visually recognizable pattern of characteristics, and in July 1993, the first baby in the world to receive a diagnosis of FAS at birth celebrated his 20th birthday (figure 1).(figure 1 omitted) Children with similar characteristics had been independently identified in France (Lemoine et al. 1968) and in Seattle (Jones et al. 1973) as a specific subgroup of children born to alcoholic mothers. The characteristics of FAS were identified as growth deficiency; specific physical anomalies, including a characteristic facies (figure 2); and central nervous system (CNS) dysfunction. The CNS manifestations include delayed development, hyperactivity, motor incoordination, learning or attentional problems, seizures, mental retardation, and/or microcephaly (small head). These early insights on FAS suggested a biological cause for some of the problems seen in children of alcoholic(1) mothers--and indicated that these problems could be prevented if women did not drink alcohol during pregnancy. Two decades of laboratory research have validated these early findings on the causes of FAS. For example, experimental research has shown that alcohol is teratogenic(2) across a wide variety of species and conditions of exposure, and it is the most commonly used known human teratogen in the world. Alcohol also causes FAS, with an estimated prevalence of 1-3/1,000 live births (National Institute on Alcohol Abuse and Alcoholism 1990). EARLY RESEARCH AND PREVENTION EFFORTS The early clinical reports of FAS by Lemoine and colleagues (1968) in western France and Jones and colleagues (1973) in Seattle were soon replicated by reports by Majewski and colleagues (1976) in western Germany, by Dehaene and colleagues (1977a) in northern France, and by Olegard and colleagues (1979) in Sweden. Like the initial reports, all of these studies in the 1970's described patients with FAS who were infants and young children. Because these children with FAS were mostly functioning within the borderline and retarded range of intellectual development. FAS soon became recognized as one of the three most prevalent causes of mental retardation with a known etiology-and the only one that was entirely preventable. This knowledge stimulated the development of important programs in the late 1970's, designed to demonstrate methods to prevent FAS and to intervene in maternal alcohol abuse during pregnancy (Rosen et al. 1980; Rosett and Weiner 1981; Little and Streissguth 1981; Little et al. 1984, 1985). The United States Government initiated two important policies: an official government warning by the Surgeon General against drinking alcoholic beverages during pregnancy or when planning a pregnancy (Public Health Service 1981), and the labeling of alcoholic beverage containers with a warning about the risk of birth defects associated with drinking alcohol during pregnancy (Public Law 100-690, 1988). …

A Long-Term Perspective of FAS

The frequencies of 60 minor physical anomalies and various craniofacial measurements in 52 children with alcohol exposure of various durations in utero were determined and compared with 48 non-exposed healthy children at a mean age of 27 months. Compared with non-exposed children a significantly higher total minor physical anomaly count was observed in those children exposed prenatally to alcohol throughout pregnancy. Binge drinking was not associated with an increased minor physical anomaly count. During the first year of life facial features were judged according to subjective impression: 10 children had typical facial features of fetal alcohol syndrome (FAS) and 19 children were judged to have possible fetal alcohol effects on their face. Only six of them fulfilled the strict craniofacial criteria for diagnosis of FAS at the age of 27 months. Our results stress the importance of recognising also the subtle dysmorphic facial features associated with prenatal alcohol exposure: 22 of 29 (76%) of exposed children judged to have typical or possible features of FAS during the first year showed signs of central nervous system dysfunction at the age of 27 months.

https://adc.bmj.com/content/archdischild/67/6/712.full.pdf

Dysmorphic features in offspring of alcoholic mothers.

68 cases of alcohol embryopathy are reported. The main symptoms are intrauterine and postnatal growth retardation (91%), microcephaly (87 per cent), psychomotor and mental retardation (84 per cent) and a typical craniofacial dysmorphism. Other malformations are frequently found such as cardiac defects (31 per cent), anomalies of joints (23 per cent) and genitalia (50 per cent). There is a marked variation in the intensity of the malformations. Taking into account the extent of the craniofacial dysmorphism and the cerebral damage, a classification into three types (I-111) of alcohol embryopathy is proposed. That ethanol has a teratogenic effect seems to be confirmed. The mother's clinical history suggests that the quantity of alcohol consumed has no marked influence on birth weight, length of gestation and severity of the symptoms. Possibly a defective ethanol metabolism in the severely affected mothers may account for the dysplasias.

[Clinical aspects of pathogenesis of alcohol embryopathy (author's transl)].

[Alcoholic embryopathy, a frequent intrauterine damage].

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[Clinical aspects of pathogenesis of alcohol embryopathy (author's transl)].

[Alcoholic embryopathy, a frequent intrauterine damage].