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Results for “Fetal Alcohol Spectrum Disorders”

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PubMed1978

The fetal alcohol syndrome: symptoms and pathogenesis.

The symptoms of the fetal alcohol syndrome and their frequency of appearance are described based on 41 reports in the literature and on own observations. Experimental evidence is presented proving the lack of cytotoxicity, mutagenicity and teratogenicity of alcohol itself and the intensive cytotoxicity, mutagenicity and teratogenicity of acetaldehyde. Responsibility for the fetal alcohol syndrome is ascribed to acetaldehyde at maternal blood concentrations surpassing 35 micrometer and it is suggested that the raised acetaldehyde level is due to an inherited or acquired defect of mitochondrial aldehyde dehydrogenase. Prospective mothers displaying acetaldehyde levels exceeding 30 micrometer after a drink should be advised against bearing a child.

Abnormalities, Drug-Induced↗
PubMed1993

Ethanol-induced teratogenic alterations in developing cardiomyocytes in culture.

The development of an in vitro cardiogenesis model was designed to enhance our understanding of the mechanism(s) of ethanol teratogenicity. Growth and development events in the model are similar to in vivo events. Time-specific and event-specific windows of biokinetic activities during both hyperplastic and hypertrophic growth are easily controlled and independently investigated. Systematic study of the effects of ethanol on the embryogenesis model, from committed blast cells to mature, functioning cells was accomplished to determine at what stage or stages of the growth and development paradigm ethanol exerts its teratogenic potential. Using the model and comparing the data to in vivo ethanol exposures, it appears that ethanol impairs the capability of the cell to properly propagate and mature.

Animals↗
PubMed1997

Repeated exposure to moderate doses of alcohol in the rat fetus: evidence of sensitization to toxic and chemosensory aspects of alcohol.

Two experiments tested responsiveness of the rat fetus to alcohol on gestational day (GD) 20 after previous maternal administration of low-to-moderate doses of alcohol (1 or 2 g/kg during GDs 17 to 19). Maternal alcohol intoxication on GD 20 resulted in substantial suppression of spontaneous fetal motor activity. The analysis of mouthing movements showed that this suppression of movement was further enhanced by exposure to alcohol during the previous 3 days of gestation (GDs 17 to 19). A second experiment indicated that this same exposure to alcohol during GDs 17 to 19 induced fetuses on GD 20 to emit more mouthing movements in response to intraoral infusions of alcohol. A moderate amount of prenatal alcohol exposure apparently sensitizes the fetus to the pharmacological and orosensory effects of alcohol.

Animals↗
PubMed1997

Ethanol-induced changes in prostaglandin E concentration in the intact cerebral cortex of preterm and near-term fetal sheep.

Ethanol-induced changes in fetal prostaglandin E (PGE) concentration may play a role in the toxic effects of prenatal ethanol exposure. Using the novel technique of in utero microdialysis, the present study tested the hypothesis that acute ethanol exposure changes PGE concentration in the intact cerebral cortex of preterm (93 +/- 1 days of gestation) and near-term (124 +/- 1 days of gestation; term, approximately 147 days) fetal sheep. Fetal sheep were surgically instrumented with a microdialysis probe placed in the parasagittal parietal cortex. Three days later, the effects of maternal infusion of 1 g of ethanol/kg maternal body weight on preterm (n = 6) and near-term (n = 7) fetal cerebral cortical and plasma PGE concentrations were determined. In the preterm fetal cerebral cortex, PGE concentration was increased after ethanol infusion in all six animals studied. The median peak increase was 160% with a 95% confidence interval of 115 to 784%. There was considerable variation in the time of occurrence, magnitude, and duration of this increase. In the near-term fetal cerebral cortex, an increase in PGE concentration was observed after ethanol infusion in 5 of the 7 animals studied, whereas a decrease in PGE concentration was observed in the other two animals. Overall, ethanol did not increase significantly near-term fetal cerebral cortical PGE concentration. For both age groups, ethanol infusion had no effect on fetal plasma PGE concentration. These data indicate that ethanol can affect PGE production in the fetal cerebral cortex and that this effect seems to be gestational-age-dependent.

Animals↗
PubMed1997

Effect of prenatal ethanol exposure on fetal calcium metabolism.

Alcohol consumption has adverse effects on both adult and developing bone. The mechanisms by which alcohol affects bone, however, are unknown. This study examined the possibility that maternal alcohol consumption may affect fetal bone development by altering fetal levels of parathyroid hormone (PTH), 1,25(OH)2D, or calcitonin (hormones that regulate calcium (Ca) and bone metabolism in the adult animal). Female Sprague-Dawley rats were bred and divided into three groups: 1 group was fed lab chow ad libitum (Control; C) and the other 2 groups received a liquid diet with (Ethanol; E) or without (Pair-fed; PF) ethanol. Blood from dams and fetuses was collected on day 21 of gestation, and selected fetuses were stained for determination of the degree of bone ossification. Mean fetal body weight and fetal skeletal ossification were reduced in the E compared with PF and C groups. Total Ca levels in fetal serum, however, showed a trend to be increased in E compared with PF and C fetuses, and no significant group differences were found in fetal serum levels of albumin, PTH, or calcitonin. Serum levels of 25-OH-D and 1,25(OH)2D were significantly decreased in E and PF, compared with C fetuses. Total Ca levels in maternal serum did not vary with the group; however, serum albumin levels were higher in E, compared with PF and C dams, suggesting that serum ionic Ca levels may have been reduced in the E dams. Serum levels of 25-OH-D were reduced in the E, compared with PF and C dams, whereas levels of 1,25(OH)2D were elevated. PTH levels did not vary among groups. Interestingly, serum calcitonin levels were elevated in the E, compared with PF and C, dams. These results indicate that the effects of ethanol on fetal bone development do not appear to be related to alterations in fetal serum levels of PTH, 1,25(OH)2D, or calcitonin. Maternal ethanol consumption, however, results in reduced appetite and a decrease in dietary Ca intake. Despite the reduced Ca intake, the ability of the dam to maintain Ca homeostasis appeared intact, although this may be dependent on the duration of ethanol consumption.

Alcohol Drinking↗
PubMed1999

Fetal syndromes and the charter: the Winnipeg glue-sniffing case.

The relationship between scientific knowledge and legal discourse is raised once again by a recent decision of the Supreme Court of Canada, a case involving a young Aboriginal woman who was pregnant and ordered by the court to remain in a drug treatment program at a health center until the baby was born. Her glue-sniffing habit was deemed dangerous to the normal development of the fetus. The Court held that her solvent-dependency did not justify the original court action, but both the Court and the various interveners disregarded the current state of our knowledge on the fetal syndromes. There is thus a continuing disconnect between the scientific understanding of fetal risk and the development of Constitutional law around women's reproductive rights. This paper reviews the case and follows it through the appellate process; we examine the research literature on fetal syndromes tracking the changes over time. Finally we comment on the interventions by the Winnipeg Child and Family Services, the Women's Health Rights Coalition, by The Canadian Civil Liberties Association, and both The Canadian Abortion Rights Action League and the Women's Legal Education and Action Fund.

Adult↗
PubMed1987

[Embryopathic-dysontogenetic syndromes in pathocharacterological disorders in the progeny of alcoholic parents].

In a clinical and follow-up study of the progeny of alcoholic parents the author investigated embryopathic/dysontogenetic disorders ("oligosymptomatic" forms of alcoholic embryopathy, mental infantilism, hyperdynamic syndrome and the syndrome of cerebrospinal fluid hypertension) exerting a pathoplastic effect on the deviant behaviour of adolescents. The author has developed approaches toward a multiple modality therapy and rehabilitation of these patients in conditions of a special school for adolescents with deviant behaviour. A hypothesis is advanced as to the relationship between embryopathic/dysontogenetic disorders with embryofetotoxic effect of the mother's alcoholism on the fetus during pregnancy.

Adolescent↗
PubMed2005

Prenatal alcohol and drug exposures in adoption.

Prenatal alcohol and drug exposures are a significant concern in many domestic and international adoptions. This article addresses the following substance exposures for children: alcohol, opiates, tobacco, marijuana, cocaine, and methamphetamines. For each substance, we review the teratogenicity of the exposure and identify the spectrum of neurodevelopmental issues that can present in children exposed to this substance. Diagnosis of the spectrum of fetal alcohol outcomes is also discussed. When possible, we provide country-specific statistics on exposure risks for adopted children.

Adoption↗
PubMed1983

Epidemiology of mental retardation--a Swedish survey.

ecent epidemiological studies in Swedish school age children revealed a prevalence of severe mental retardation (SMR = IQ less than 50) of 0.3% and of mild mental retardation (MMR = IQ 50-70) around 0.4%. In SMR prenatal causes were found in 55%, perinatal in 15-20%, no traceable brain pathology in 18%. Corresponding figures for MMR were 23%, 18% and 55%, respectively. Down syndrome was the largest single cause of SMR and polygenic subcapacity considered to be that of MMR. Chromosomal errors were detected among 29% SMR and 4% MMR school children. Fragile X accounted for 4% SMR and 10% MMR in boys. Fetal alcohol syndromes constituted 8% of urban MMR. The contribution of inborn errors of metabolism was 4-5% and less than 1%, in SMR and MMR, respectively. Perinatal (28th prenatal week-28th postnatal day) brain damage was implicated in 15% of SMR and 18% of MMR. Pathogenetic data are considered for potential preventive measures.

Adolescent↗
PubMedDate not supplied

The adult antisocial syndrome with and without antecedent conduct disorder: comparisons from an adoption study.

DSM antisocial personality disorder (ASPD) requires a retrospective diagnosis of conduct disorder-historical behavior not present in everyone with adult ASPD criteria. Using adoption study data, we examined the impact of this requirement on biological and environmental risk associations. We also compared clinical correlates of adult antisocial behavior with and without prior conduct disorder. We defined three subgroups: DSM-III ASPD (n = 30), adult antisocials without conduct disorder (n = 25), and controls (n = 142). By design, the sample had a high incidence of biological parent ASPD, which was partially confounded with fetal alcohol exposure. We compared the associations of both of these putative risk factors with subgroup membership after controlling for gender and adverse adoptive environment. We also examined differences in two sociopathy scales and the incidence of co-occurring affective, alcohol, and other substance use disorders. Finally, we explored differences in individual antisocial symptoms. Having an antisocial biological parent was a specific risk factor for ASPD. In contrast, fetal alcohol exposure, male gender, and adverse environment were associated with the adult antisocial syndrome, regardless of conduct disorder history. The two antisocial groups were similar with respect to sociopathy scales, co-occurring diagnoses, and the incidence of most individual symptoms. However, several adult and conduct disorder symptoms had significant specific associations with biological or environmental background or their interaction. Phenotypic expression of the biological-possibly genetic-risk for ASPD appears to be manifest before adulthood. The influence of other risk factors may not depend on antecedent conduct disorder. Despite this, we could not detect clinically important differences between the two sociopathic groups. The conduct disorder requirement therefore may be more relevant to etiological than clinical understanding of adult antisocial behavior.

Adolescent↗
PubMed2002

Psychiatric illness in a clinical sample of children with prenatal alcohol exposure.

The purpose of this study was to describe psychiatric disorders exhibited by children with prenatal alcohol exposure. Twenty-three children between the ages of 5 and 13 years who were referred to the UCLA Fetal Alcohol and Related Disorders Clinic because of heavy exposure to alcohol in utero were evaluated. Children with intelligence quotients of 70 and above and their families were interviewed by the study child psychiatrist and psychologist and psychiatric diagnoses were based upon DSM-IV diagnostic criteria. Inter-observer reliability of diagnosis was established comparing clinical diagnoses with diagnoses made using the "best-estimate" procedure. For the best estimate method, items from the Child Behavior Checklist, the Fetal Alcohol Behavior Scale, the Child Symptom Inventory-4, the Conners' Rating Scale, as well as information from historical records were reviewed by two experienced clinicians who were blind to the diagnostic and alcohol exposure status of the children. Approximately 87% of the sample met criteria for a psychiatric disorder. The majority of the children (61%) were assigned a mood disorder diagnosis. Twenty-six percent were diagnosed with major depressive disorder or adjustment disorder with depressed mood and 35% met criteria for bipolar disorder. Psychiatric disorders are common in children with prenatal alcohol exposure. In particular, these children seem to be highly vulnerable to mood disorders. There is a need for training in how to recognize the physical and behavioral phenotypes of children with prenatal alcohol exposure so that appropriate treatment can be initiated early.

Adolescent↗
PubMed1995

Specific impairments in self-regulation in children exposed to alcohol prenatally.

The present study utilizes a conceptual framework derived from theories of cognition to explain the pattern of behavioral and learning problems observed in subjects with fetal alcohol syndrome (FAS) and fetal alcohol effects (FAE). Based on a modern interpretation of Luria's theory of self-regulation, this study used a neuropsychological test battery to compare 10 subjects (mean age = 13 years) having FAS/FAE with 10 control subjects (mean age = 12 years and 9 months). Subjects with FAS/FAE were relatively high functioning and did not significantly differ from controls with respect to receptive vocabulary. However, those with FAS/FAE exhibited greater difficulty than controls on tasks that involved the manipulation of information and goal management in working memory (e.g., Planning, Controlled Oral Word Association, etc). Both groups performed equally well on some tasks that demanded rule learning (Delayed Response) and response inhibition (Go-No-Go). The above impairments were interpreted to be reflective of selective rather than generalized disruptions of neural networks that subserve working memory.

Adolescent↗
PubMed2006

The alcoholism generator.

Alcohol exposure largely affects 3 populations: fetuses, adolescents, and adults. These 3 developmental stages are inextricably intertwined such that elevated alcohol exposure at any time increases the probability of exposure at the others. This circular interdependency is called the alcoholism generator. Furthermore, exposure to large amounts of alcohol at these 3 times can cause cognitive dysfunction, largely through mechanisms of alcohol-induced perturbations in neurogenesis and synaptogenesis. Breaking this cycle is key to reducing problem alcohol drinking and the associated sequelae.

Adolescent↗