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Results for “Fetal Alcohol Spectrum Disorders”

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PubMed2002

Neurological basis of deficits in affective prosody comprehension among alcoholics and fetal alcohol-exposed adults.

Affective prosody is a nonlinguistic aspect of language that conveys emotions and attitudes during discourse. In this study the neurological basis of affective prosodic comprehension (APC) dysfunction in alcoholics (ALC) and fetal alcohol-exposed adults (FAexp) was explored. Subjects were previously tested for APC by use of the Aprosodia Battery, including 9 right-brain-damaged and 10 left-brain-damaged subjects. ALC and FAexp subjects were significantly less accurate than control subjects in APC, and scored similarly to patients with focal brain lesions. The specific APC impairment found in ALC and FAexp may be a consequence of both callosal and right cortical dysfunction or damage.

Adult↗
PubMed1984

Alcohol use during pregnancy.

Heavy alcohol intake during pregnancy is associated with numerous adverse effects on the fetus, including low birth weight, congenital anomalies, mental retardation, and behavioral and learning disabilities. There is increasing evidence that moderate drinking also may cause these problems, but to a lesser degree. Less is known about the effects of a single drink or a single alcoholic binge, but no absolutely safe level of alcohol consumption has been determined for pregnant women.

Abnormalities, Multiple↗
PubMed1982

Development and psychopathology of children with the fetal alcohol syndrome.

Extended psychiatric and pediatric examinations were performed on patients with the fetal alcohol syndrome (FAS). A subgroup of these patients underwent psychological testing to measure intelligence, visual perception, and psycholinguistic abilities. Psychopathology was also studied in a matched control group. The investigation revealed a broad scale of developmental hazards and psychopathologic symptoms indicating the negative long-range effects of alcohol abuse during pregnancy. The extent of morphologic damage was found to be a good predictor of psychopathology and mental impairment. Social environment and socioeconomic status appear less important as predictors.

Abnormalities, Drug-Induced↗
PubMed2000

Acute psychiatric disturbance in pregnancy and the puerperium.

Psychiatric disturbance occurring during pregnancy or the puerperium can occur as a first presentation or as a recurrence or deterioration of a previously diagnosed psychiatric illness. Whatever the history or aetiology, the occurrence of psychiatric disturbance during this period can have profound, long-term implications not only for the mental health of the mother, but also for her relationship with her child and other family members, as well as for the child's development. The treatment of psychiatric disturbance at this time can present difficult dilemmas and should always involve a careful analysis of the risks and benefits of treatment. Liaison between obstetricians and psychiatrists is to be strongly encouraged in order to ensure the best possible outcome for both mother and baby. The antenatal period offers a unique opportunity to identify individuals at risk and target them in order to promote psychological well-being during pregnancy and the puerperium.

Antidepressive Agents↗
PubMed1998

A review of the neurobehavioral deficits in children with fetal alcohol syndrome or prenatal exposure to alcohol.

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.

Alcohol Drinking↗
PubMed2005

Impaired cerebellar learning in children with prenatal alcohol exposure: a comparative study of eyeblink conditioning in children with ADHD and dyslexia.

Neuroanatomical and behavioral evidence indicate that the cerebellum is particularly vulnerable to the toxic effects of prenatal alcohol exposure. Recent research has shown impairments in eyeblink conditioning in rats following binge-like neonatal ethanol exposure. The neural substrates of eyeblink conditioning have been localized to the cerebellum and related brainstem mechanisms. The present study considered whether heavy prenatal alcohol exposure would result in similar impairments in eyeblink conditioning in children. A related purpose was to determine if eyeblink conditioning could discriminate between children with prenatal alcohol exposure and children diagnosed with attention deficit hyperactive disorder or developmental dyslexia. Fifty-three age-matched children [10 prenatal alcohol exposure (FAE), 16 attention deficit hyperactive disordered (ADHD), 14 children with dyslexia (DYS), 13 normal controls] were assessed on eyeblink conditioning in the delay paradigm. Children in the FAE and DYS groups failed to learn the conditioned response, producing longer latencies and poorly timed responses to the conditioning stimulus. Children with ADHD were impaired on measures of adaptively timed responses, although conditioned responses matched normal controls. The results suggest that children prenatally exposed to alcohol have deficits in cerebellar processing similar to those with dyslexia, and that these functional deficits are related to disabilities in learning.

Alcohol Drinking↗
PubMed1997

Heavy prenatal alcohol exposure with or without physical features of fetal alcohol syndrome leads to IQ deficits.

OBJECTIVE: To assess general intellectual functioning in children with histories of heavy prenatal alcohol exposure, with or without the facial features and growth deficiencies characteristic of fetal alcohol syndrome (FAS). DESIGN: Forty-seven alcohol-exposed children were recruited on evaluation at a dysmorphology clinic and evaluated as part of a university research project using standard tests of IQ. Thirty-four of the alcohol-exposed patients met the traditional diagnostic criteria for FAS. The other 13 alcohol-exposed children lacked both the pattern of facial features and prenatal or postnatal growth deficiency characteristic of the diagnosis. RESULTS: Compared with normal control subjects matched for age, sex, and ethnicity, both groups of alcohol-exposed children displayed significant deficits in overall IQ measures and deficits on most of the subtest scores. Although those in the nondysmorphic group usually obtained marginally higher IQ scores than those in the FAS group, few significant differences were found between the two alcohol-exposed groups. CONCLUSIONS: These results indicate that high levels of prenatal alcohol exposure are related to an increased risk for deficits in intellectual functioning and that these can occur in children without all of the physical features required for a diagnosis of FAS. They also emphasize the need for conducting a thorough history of prenatal alcohol exposure in children with intellectual deficits.

Child↗
PubMedDate not supplied

The teratogenic effects of alcohol following exposure during pregnancy, and its influence on the chromosome constitution of the pre-ovulatory egg.

Much information has emerged over the years concerning the teratogenicity of acute and chronic alcohol exposure during pregnancy. Both alcohol and its primary metabolite, acetaldehyde, are teratogenic. Exposure during pregnancy may lead to fetal alcohol syndrome (FAS), and this is said to occur in a substantial proportion of infants born to mothers who are chronic, heavy daily drinkers. Such infants usually survive to birth but are mentally retarded, often display growth retardation and additionally display a characteristic range of clinical features, principally craniofacial abnormalities and neurological damage. We have recently been interested in the effect of exposure of pregnant female mice to a single high level of alcohol during pregnancy, equivalent to an episode of 'binge' drinking, on the optic nerve, and believe that our findings, which are outlined in the first part of this review, may shed important light on the pathogenesis of some of the ocular features characteristically seen in infants with this syndrome. What is not generally appreciated, is that exposure to alcohol and other 'spindle-active' substances that have a similar action on the meiotic spindle apparatus during the menstrual cycle before conception can induce chromosome segregation errors in the ovulated oocyte. The successful fertilization of such eggs consequently results in the production of aneuploid embryos, which have a very high chance of being spontaneously aborted during the first trimester of pregnancy. Those relatively few aneuploid conceptuses that survive to term invariably show moderate to severe degrees of mental retardation, craniofacial and other abnormalities, as well as having a significantly reduced life expectancy. The findings from our experimental studies that have been carried out in mice draw attention to important principles which are of general applicability to the situation in the human. These findings, and our conclusions drawn from them, are discussed in detail in the second part of this review.

Aneuploidy↗
PubMed1999

Identifying fetal alcohol syndrome among youth in the criminal justice system.

A disproportionately large number of youth and adults with fetal alcohol syndrome (FAS) and fetal alcohol effects (FAE) seem to be coming into conflict with the legal system. Learning and behavioral difficulties associated with FAS/FAE may make them more susceptible to criminal behavior. This study determined the prevalence of FAS/FAE among youth who were remanded for a forensic psychiatric/psychological assessment. All youth remanded to a forensic psychiatric inpatient assessment unit over a 1-year period were evaluated for FAS/FAE. Of the 287 youth, 67 (23.3%) had an alcohol-related diagnosis: 3 (1.0%) had a diagnosis of FAS and 64 (22.3%) had a diagnosis of FAE. Thus, this group is disproportionately represented in the juvenile justice system, indicating the need for increased education and awareness among those in the criminal justice system involved with these youth.

Adolescent↗
PubMed2005

Relation of prenatal alcohol exposure to cognitive processing speed and efficiency in childhood.

BACKGROUND: Prenatal alcohol exposure has been linked to deficits in processing speed in both infancy and later in childhood. This study was designed to examine prenatal alcohol-related deficits in both processing speed and processing efficiency in four domains of cognitive function. METHODS: Black children (n=337; age, 7.5 years), prospectively recruited to over-represent prenatal alcohol exposure at moderate-to-heavy levels, were assessed on four processing speed tasks, using a Sternberg paradigm. Hierarchical linear modeling was used to contrast overall processing speed, indicated by reaction time (RT) differences at the intercept, with processing efficiency, indicated by the slope of RT changes across increasing levels of task difficulty. Performance on these tasks within an effortful cognitive framework was compared with RT on a task involving relatively more automatic processing. Path analysis was used to examine the degree to which the effect of prenatal alcohol exposure on working memory was mediated by slower RT. RESULTS: Prenatal alcohol exposure was associated with slower processing speed on several of the Sternberg tasks, and the number comparison task showed a specific deficit in processing efficiency. These effects on tasks involving effortful processing contrasted with the lack of performance differences on the more automatic RT measure. The relation of prenatal alcohol exposure to working memory was mediated, in part, by an associated reduction in processing speed. CONCLUSIONS: These data confirm reports by other investigators linking prenatal alcohol exposure to slower processing speed and show that this RT deficit is found within the context of complex cognition but not where automatic processing is involved. The reduction in RT accounts, in part, for the previously reported alcohol-related effects on working memory. The number comparison slope was the only specific component of information processing affected, confirming previous reports of a distinctive prenatal alcohol effect on number processing.

Attention↗
PubMed1990

Lower serum thyroxine levels in rats following prenatal exposure to ethanol.

Fetal alcohol syndrome (FAS) is noted for poor growth, developmental delays, and mental retardation. In animals, prenatal alcohol exposure alters anatomical, physiological, and neurochemical maturation and produces behavioral changes similar to those in children. Since thyroid hormones are critical trophic factors for normal somatic and neural maturation, and since fetal thyroid hormones are profoundly affected by acute maternal ethanol administration, we hypothesized that postnatal effects of prenatal alcohol exposure may be related to abnormal thyroid hormone development. We report here that young rats exposed to alcohol in utero have significantly lower serum total thyroxine (T4) concentrations than normal and pair-fed control rats. The results suggest prenatal ethanol exposure may compromise thyroid development in ways not attributable to undernutrition or developmental delays alone. Lowered total T4 levels may be a teratogenic outcome of prenatal alcohol exposure, which could contribute to impaired growth, altered neural organization, and behavioral dysfunction.

Alcohol Drinking↗
PubMed1992

Effects of alcohol on intrauterine oxygen tension in the rat.

The effects of alcohol on the availability of oxygen within the uterine lumen of rats were determined on Day 4 of pseudopregnancy. Intraluminal oxygen tension (pO2) was measured in vivo in anesthetized rats using a 22-gauge polarographic oxygen sensor. Intrauterine pO2 was measured for 15 min before and after intravenous injection of alcohol (1.0 g/kg: 100% ethanol/saline, 1:2v/v) or vehicle (physiological saline). Alcohol administration increased mean intrauterine pO2 (mm Hg) from a pretreatment level of 28.3 +/- 2.8 to 38.7 +/- 3.8 mm Hg (p less than 0.05, n = 10) at 15 min postinjection. The rapid rise in oxygen tension was accompanied by increased frequency of fluctuation (peaks/hr) in intraluminal pO2 (prealcohol: 64.2 +/- 8.8 vs. postalcohol 96.0 +/- 7.7 peaks/hr; (p less than 0.05, n = 10). Injection of saline did not alter any aspect of intrauterine pO2. During the period of measurement of luminal pO2, blood alcohol levels increased from 0 during pretreatment to 106 mg% within 10 min of injection. These results indicate that alcohol increases the availability of oxygen within the uterus during the time of endometrial sensitivity to deciduogenic stimuli and blastocyst implantation.

Animals↗
PubMed1996

Effect of maternal ethanol consumption on maternal and fetal calcium metabolism.

Alcohol consumption can have deleterious effects on both adult and developing bone. The mechanism(s) by which alcohol affects bone, however, is unknown. This study investigated the possibility that alcohol affects bone by alterations in calcium (Ca) metabolism. Female rats were fed lab chow ad libitum (C, Control) or a liquid diet with (E, Ethanol) or without (PF, Pair-Fed) ethanol. After 2 weeks on their respective diets, the rats were bred and the experimental diets continued throughout gestation. Blood (dams only) and tissue were collected on day 21 of gestation. The Ca content of maternal bone showed a trend toward a decrease in E and PF compared with C dams. Ionic Ca (iCa) levels were decreased in the blood of the E compared with PF and C dams. Serum parathyroid hormone levels were elevated in the E compared with C dams, consistent with the low iCa levels. Serum levels of 1,25(OH)2D, however, were elevated only in the PF dams. Mean fetal body weight and fetal skeletal ossification were reduced in the E compared with PF and C groups, but no group differences were found in fetal Ca content. These results indicate that maternal ethanol consumption compromised the ability of the dam to regulate her blood iCa levels, possibly partly due to a failure to increase 1,25(OH)2D levels. The delays in skeletal development observed in the ethanol exposed fetuses, however, do not appear to result from impaired placental Ca transfer.

Animals↗
PubMed1988

Fetal alcohol syndrome in rats: conditions for improvement of ethanol effects on fetal cerebral development with supplementary agents.

As a possible preventative measure for brain dysfunction in the fetal alcohol syndrome, the effect of zinc or vitamin E supplementation together with ethanol on the fetal cerebrum was investigated in rats. Contrary to our previously published data showing the good effect of 0.01% zinc with 30% ethanol on fetuses, the administration of 0.01% zinc with 20% ethanol, 0.03% vitamin E with 20% ethanol or 0.02% vitamin E with 10% ethanol during pregnancy did not result in a good effect on the body and cerebral weights of fetuses on gestational day 21. The development of dendritic branches on frontal cerebral neurons in fetuses was decreased in the order of the control, zinc with ethanol and ethanol groups. The concentration and content of alpha-tocopherol were increased, but those of zinc were not, in the fetal cerebrum with the maternal administration of vitamin E or zinc together with ethanol, respectively. These results suggest that the improvement of the brain function might depend on the deficient agent induced by maternal ethanol ingestion.

Animals↗
PubMed2002

Some implications of prenatal alcohol exposure for the treatment of adolescents with sexual offending behaviors.

Prenatal alcohol exposure can seriously harm the fetus, resulting in a wide range of physical and central nervous system abnormalities. A follow-up study of persons prenatally exposed to alcohol found that 49% of adolescents and adults had repeatedly displayed inappropriate sexual behavior. While these persons are likely to present to sexual offender treatment programs, they are unlikely to be recognized as neurologically impaired because the sequelae of prenatal alcohol exposure are seldom accurately identified by clinicians. Persistent impairments in response inhibition, memory, and executive functions are common, requiring adaptations to standard sexual offender assessment and treatment.

Adolescent↗