UNSW Embryo- Abnormal Development-Fetal Alcohol Syndrome.Selected References |
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Note: A Selected List of References for Fetal Alcohol Syndrome from PubMed April 1999 back. |
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Internet access computers will be able to get abstract directly from PubMed (when available) by clicking Author's name below. If the Journal is available online then this is also listed at the end of the Reference citation. |
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Articles
- AMERICAN ACADEMY OF PEDIATRICS Policy
Statement Fetal
Alcohol Syndrome and Fetal Alcohol Effects (RE9310)
Pediatrics Volume 91, Number 5 May, 1993, p
1004-1006.
- Neuropsychological deficits in adolescents with
fetal alcohol syndrome: clinical findings. Olson
HC, Feldman JJ, Streissguth AP, Sampson PD, Bookstein
FL Alcohol Clin Exp Res 1998 Dec;22(9):1998-2012
- Abstract Understanding the nature of
cognitive deficits among adolescent patients with
fetal alcohol syndrome (FAS) can direct future
research on assessment and intervention. In an
exploratory study, nine nonretarded teenagers with FAS
were administered tests of IQ and adaptive behavior,
and neuropsychological tests presumed sensitive to
alcohol effects. Their performance was compared with
psychometric norms and to data from a sample of 174
adolescents with minimal or no prenatal alcohol
exposure. These nonretarded FAS patients commonly
showed behavior problems, decreased social competence,
and poor school performance. Neuropsychological
testing revealed significant deficits, although no one
neuropsychological profile characterized all patients
and not all tests revealed problems. Relatively intact
performance was observed in procedural memory, some
measures of reaction time, and some reading measures.
Deficits were seen on attentional and memory tasks
tapping visual-spatial skills, short-term auditory
attention and memory, declarative learning, and
cognitive flexibility and planning. Difficulties in
processing speed and accuracy were also seen.
Comparison with a subgroup of 52 nonalcohol-exposed or
minimally alcohol-exposed adolescents with a similar
range of IQ scores demonstrated that deficits among
these FAS patients were not fully explained by a
general lowering of IQ.
- Abstract Understanding the nature of
cognitive deficits among adolescent patients with
fetal alcohol syndrome (FAS) can direct future
research on assessment and intervention. In an
exploratory study, nine nonretarded teenagers with FAS
were administered tests of IQ and adaptive behavior,
and neuropsychological tests presumed sensitive to
alcohol effects. Their performance was compared with
psychometric norms and to data from a sample of 174
adolescents with minimal or no prenatal alcohol
exposure. These nonretarded FAS patients commonly
showed behavior problems, decreased social competence,
and poor school performance. Neuropsychological
testing revealed significant deficits, although no one
neuropsychological profile characterized all patients
and not all tests revealed problems. Relatively intact
performance was observed in procedural memory, some
measures of reaction time, and some reading measures.
Deficits were seen on attentional and memory tasks
tapping visual-spatial skills, short-term auditory
attention and memory, declarative learning, and
cognitive flexibility and planning. Difficulties in
processing speed and accuracy were also seen.
Comparison with a subgroup of 52 nonalcohol-exposed or
minimally alcohol-exposed adolescents with a similar
range of IQ scores demonstrated that deficits among
these FAS patients were not fully explained by a
general lowering of IQ.
- Fetal alcohol syndrome: the
'American Paradox'. Abel
EL Alcohol and Alcoholism: International Journal of
the Medical Council on Alcoholism 1998
May-Jun;33(3):195-201
- This study examined alcohol consumption and the
incidence of fetal alcohol syndrome (FAS). The
"American paradox" reveals that even though Americans
have a relatively low rate of per capita alcohol
consumption, the United States has the highest
incidence of FAS in the world; the incidence of FAS in
the U.S. is about 20 times higher than it is for all
of the rest of the world combined. Per capita alcohol
consumption, however, may be misleading in terms of
its relation to FAS, since per capita data are based
on the total adult population in a country and include
men and women. Men are not only more likely to be
alcohol consumers than women, they also typically
drink more than women, and have a higher prevalence of
alcohol abuse. An alternative way of exploring the
"American paradox" is to compare rates of drinking
among women in various countries and especially the
number of women who drink during pregnancy. Such a
comparison revealed that an almost identical
percentage of American women drink prior to, and
during pregnancy (68 and 49 percent respectively),
compared to those in European countries and
Australia/New Zealand (69 and 49 percent,
respectively). With respect to the incidence of FAS
among "heavy" drinkers, data indicate that the
incidence of FAS increases to 4 percent when one
focuses on women who are selected on the basis of
"heavy" drinking during pregnancy. Several
explanations of the "American paradox" are discussed,
including the impact of low socioeconomic status on
alcohol consumption and FAS.
- This study examined alcohol consumption and the
incidence of fetal alcohol syndrome (FAS). The
"American paradox" reveals that even though Americans
have a relatively low rate of per capita alcohol
consumption, the United States has the highest
incidence of FAS in the world; the incidence of FAS in
the U.S. is about 20 times higher than it is for all
of the rest of the world combined. Per capita alcohol
consumption, however, may be misleading in terms of
its relation to FAS, since per capita data are based
on the total adult population in a country and include
men and women. Men are not only more likely to be
alcohol consumers than women, they also typically
drink more than women, and have a higher prevalence of
alcohol abuse. An alternative way of exploring the
"American paradox" is to compare rates of drinking
among women in various countries and especially the
number of women who drink during pregnancy. Such a
comparison revealed that an almost identical
percentage of American women drink prior to, and
during pregnancy (68 and 49 percent respectively),
compared to those in European countries and
Australia/New Zealand (69 and 49 percent,
respectively). With respect to the incidence of FAS
among "heavy" drinkers, data indicate that the
incidence of FAS increases to 4 percent when one
focuses on women who are selected on the basis of
"heavy" drinking during pregnancy. Several
explanations of the "American paradox" are discussed,
including the impact of low socioeconomic status on
alcohol consumption and FAS.
- A fetal alcohol behavior scale. Streissguth
AP, Bookstein FL, Barr HM, Press S, Sampson PD
Alcohol Clin Exp Res 1998 Apr;22(2):325-33
- Absrtact This research aimed to develop a Fetal Alcohol Behavior Scale (FABS) that describes the behavioral essence of fetal alcohol syndrome (FAS) and fetal alcohol effects (FAE), regardless of age, race, sex, and IQ. Using a reference sample of 472 diagnosed patients with FAS or FAE, ages 2 to 51, five studies are described. The FABS demonstrates high item-to-scale reliability (Cronbach's alpha = 0.91) and good test-retest reliability (r = 0.69) over an average interval of 5 years. It identifies many of the subjects with known or presumed prenatal alcohol exposure in detection studies using both prison and general samples. FABS scores also predict dependent living among adult patients with FAS/FAE. The FABS is uncorrelated with IQ, sex, age, race, and diagnosis (FAS versus FAE). We outline areas of further work to define the specificity and utility of this FABS.
- Alcohol promotes in vitro
chondrogenesis in embryonic facial mesenchyme.
Hoffman LM, Kulyk WM Int J Dev Biol 1999
Mar;43(2):167-74
- Ethanol is a well-recognized teratogen in vertebrates that can perturb the development of thefacial primordia and various other embryonic structures. However,the mechanisms underlying alcohol's effects on embryogenesis are currently unclear. Recent evidence suggests that the cranial neural crest, which forms the entire facial skeleton, may be a particularly sensitive target of ethanol teratogenicity. In the present study we have examined the influence of in vitro ethanol exposure on cartilage differentiation in micromass cultures of mesenchymal cells isolated from the various facial primordia (maxillary, mandibular, frontonasal, and hyoid processes) of the stage 24 chick embryo. In all four populations of facial mesenchyme, exposure to 1-1.5% ethanol promoted marked increases in Alcian blue-positive cartilage matrix formation, a rise in 35SO4 accumulation into matrix glycosaminoglycans, and enhanced expression of cartilage-characteristic type II collagen and aggrecan gene transcripts. In frontonasal and mandibular mesenchyme cultures, which undergo extensive spontaneous cartilage formation, ethanol treatment quantitatively elevated both matrix production and cartilage-specific gene transcript expression. In cultures of maxillary process and hyoid arch mesenchyme, which form little or no cartilage spontaneously, ethanol exposure induced the formation of chondrogenic cell aggregates and the appearance of aggrecan and type II collagen mRNAs. These actions were not restricted to ethanol, since tertiary butanol treatment also enhanced cartilage differentiation in facial mesenchyme cultures. Our findings demonstrate a potent stimulatory effect of alcohol on the differentiation of prechondrogenic mesenchyme of the facial primordia. Further analysis of this phenomenon might yield insight into the developmental mechanisms underlying the facial dysmorphologies associated with embryonic ethanol exposure.
- PMID: 10235393, UI: 99249472
Reviews
- A review of the
neuroanatomical findings in children with fetal alcohol
syndrome or prenatal exposure to alcohol.
Roebuck TM, Mattson SN, Riley EP Alcohol Clin Exp Res 1998 Apr;22(2):339-44- Abstract Human and animal studies have clearly demonstrated that alcohol is both a physical and behavioral teratogen and that heavy prenatal alcohol exposure can lead to a distinct pattern of birth defects termed the fetal alcohol syndrome. Underlying the behavioral and cognitive anomalies seen in fetal alcohol syndrome are alterations in brain structure and/or function. This paper reviews the literature examining brain anomalies attributable to prenatal alcohol exposure, beginning with a survey of autopsy studies and leading up to current findings using magnetic resonance imaging and positron emission tomography studies. Autopsy reports clearly illustrate the wide and devastating influence alcohol has on the developing brain, although for the most part no specific pattern of brain malformation has been identified. More recent magnetic resonance imaging studies, particularly when combined with quantitative analysis, have indicated that specific brain areas--such as the basal ganglia, the corpus callosum, and parts of the cerebellum--might be especially susceptible to alcohol's teratogenic effects. Further studies using functional brain imaging techniques may provide even more information about the unique effects prenatal alcohol exposure has on the developing brain. Discovering specific areas of the brain that are affected by alcohol may allow clinicians and researchers to look for patterns of vulnerable regions in the brain, thereby helping in the future detection of children who are prenatally exposed to alcohol.
- Hearing, speech, language, and
vestibular disorders in the fetal alcohol syndrome: a
literature review. Church
MW, Kaltenbach JA Alcohol Clin Exp Res 1997
May;21(3):495-512.
- Abstract Fetal alcohol syndrome (FAS) is characterized in part by mental impairment, as well as craniofacial and ocular anomalies. These conditions are traditionally associated with childhood hearing disorders, because they all have a common embryonic origin in malformations of the first and second branchial arches, and have similar critical periods of vulnerability to toxic insult. A review of human and animal research indicates that there are four types of hearing disorders associated with FAS. These are: (1) a developmental delay in auditory maturation, (2) sensorineural hearing loss, (3) intermittent conductive hearing loss due to recurrent serous otitis media, and (4) central hearing loss. The auditory and vestibular systems share the same peripheral apparatuses (the inner ear and eighth cranial nerve) and are embryologically and structurally similar. Consequently, vestibular disorders in FAS children might be expected. The evidence for vestibular dysfunction in FAS is ambiguous, however. Like other syndromes associated with craniofacial anomalies, hearing disorders, and mental impairment, FAS is also characterized by a high prevalence of speech and language pathology. Hearing disorders are a form of sensory deprivation. If present during early childhood, they can result in permanent hearing, language, and mental impairment. Early identification and intervention to treat hearing, language, and speech disorders could therefore result in improved outcome for the FAS child. Specific recommendations are made for intervention and future research.
- DNA damage, DNA repair, and
alcohol toxicity--a review.
Brooks PJ Alcohol Clin Exp Res 1997 Sep;21(6):1073-82- Abstract Alcohol (ethanol) is clearly a toxic substance when consumed in excess. Chronic alcohol abuse results in a variety of pathological effects, including damage to the liver and brain, as well as other organs, and is associated with an increased risk of certain types of cancers. Alcohol consumption by pregnant women can result in fetal alcohol effects and fetal alcohol syndrome. All of these toxic effects are well documented. What is needed at present is a complete understanding of the molecular mechanisms by which alcohol causes these toxic effects. Such an understanding may lead to better treatments of some of these toxic effects. This review, focuses on the possibility that toxic effects of ethanol are mediated, at least in part, by damage to DNA. In particular, I emphasize data on the production of endogenous DNA-damaging molecules as a result of alcohol consumption and metabolism. Specific examples of DNA-damaging molecules to be considered are reactive oxygen species, including oxygen radicals, lipid peroxidation products, and acetaldehyde. The relevant DNA repair pathways that protect cells against DNA damage produced by these molecules will also be reviewed. The goal of this review is to integrate recent results from the fields of mutagenesis and DNA repair with the alcohol toxicity literature, with the aim of stimulating research into the role of DNA damage in different types of alcohol toxicity and the role of DNA repair in protecting cells from alcohol-related damage.