The parietal lobe has been shown to be one of the regions most affected by prenatal alcohol exposure. Functional domains dependent on intact parietal functioning, including mathematical and visuospatial ability, have been consistently implicated in fetal alcohol spectrum disorders. This thesis examines, in children, using blood oxygenation level dependent (BOLD) functional Magnetic Resonance Imaging, the effect of prenatal alcohol exposure on brain activation during symbolic and nonsymbolic number processing, and place learning in a virtual environment. These functional domains were investigated using tasks of proximity judgment and exact addition to assess neural correlates of symbolic number processing in 65 children (mean age ± SD = 9.45 ± 0.42 years), nonsymbolic number comparison at varying difficulties in 34 children (11.55 ± 1.15 years), and place learning in a virtual reality computer generated (CG) arena in 57 children (9.44 ± 0.42 years; 29 boys). In the symbolic number processing tasks greater prenatal alcohol exposure was related to less activation in the right horizontal intraparietal sulcus known to mediate mental representation and manipulation of quantity. Children with fetal alcohol syndrome and partial fetal alcohol syndrome appeared to compensate for this deficit by increased activation of the left angular gyrus during the proximity judgment task. Syndromal children with fetal alcohol syndrome or partial fetal alcohol syndrome also demonstrated poor recruitment of the right horizontal intraparietal sulcus during nonsymbolic number comparison, indicating that mental representation and manipulation of quantity are impaired in children with heavy prenatal alcohol exposure, irrespective of the representation format used. This impairment was compensated for by the left angular gyrus, with only exposed children needing to recruit the left angular gyrus to a greater extent as number comparison task difficulty increased. Further, reduced activation of the right posterior superior parietal lobule in children with increasing prenatal alcohol exposure suggests that exposed children may be less able to employ the attentional systems associated with number processing. Notably, activation of nonsyndromal heavily exposed children was impaired in the right posterior superior parietal lobule, but spared in the right horizontal intraparietal sulcus. In boys only, prenatal alcohol exposure was associated with poorer place learning and reduced activation during place learning in the precuneus and posterior cingulate, as well as parahippocampal gyrus, frontal and temporal lobes, caudate, insula, claustrum, lentiform nucleus and thalamus. In girls, prenatal alcohol exposure was not associated with place learning performance or activation during place learning in any regions. These results confirm that boys and girls use different navigation strategies that rely on different brain regions and suggest that the regions used by boys are more susceptible to alcohol damage, while the regions used by girls are relatively spared. In conclusion, all the tasks investigated showed prenatal alcohol exposure related alterations in parietal function, with the impairments being widespread throughout the parietal lobe bilaterally. Notably, activation of the bilateral precuneus was affected by prenatal alcohol exposure in both the spatial navigation and nonsymbolic number comparison tasks. It is possible that this is a key region linking the deficits in number processing and visuospatial skills in children with prenatal alcohol exposure.

Alcohol is a major public health problem globally. According to the World Health Organization (WHO) report, alcohol accounts for 2.5 million deaths (4% of total) and 69.4 million (4.5% of total) of Disability-Adjusted Life Years (DALYs), (WHO, 2002, 2011). In South Africa, alcohol was found to be the third highest contributor to death and disability (Parry, 2007/8). Among the many far-reaching consequences of alcohol use in South Africa, Fetal Alcohol Syndrome (FAS) in certain regions in the country, rates among the highest in the world (May et al., 2007). Despite higher comparative levels of FAS in rural areas, almost one third of the population in urban sites (Gauteng) demonstrates that FAS is not exclusively a problem of South African rural areas. This study hypothesized that higher knowledge levels about the effects of alcohol on pregnancy may deter use among women. Employing secondary data analysis from a 2006 cross-sectional household survey, this study explored the prevalence of alcohol use among urban women (18-44 years) in the Tshwane Municipality, in general and in pregnancy. It also examined the relationship between knowledge of alcohol effects on pregnancy and alcohol use. A significant association was found between employment status, pregnancy outcome and general alcohol use among women. An almost significant association was found between knowledge of alcohol effects on pregnancy and past month alcohol use, knowledge levels and alcohol use during pregnancy. Findings partially support the hypothesis. However, knowledge of alcohol effects on pregnancy alone cannot deter women from using alcohol. Multiple influencing factors should be considered in planning prevention programmes for urban women’s alcohol use. Further research with larger sample sizes of pregnant women is suggested to explore the associations conclusively.

No description available.

Background: Fetal alcohol syndrome (FAS) is a devastating disorder whose mechanisms may be best investigated using animal models. Here we present a novel zebrafish FAS model to investigate the effects of low to moderate alcohol exposure during early development on learning. Methods: At 24-hours postfertilization zebrafish embryos were exposed to low doses of ethanol (external concentrations = 0.00, 0.25, 0.50, 0.75 and 1.00% vol/vol) for a very short duration (2 hours). Upon adulthood associative learning in the zebrafish was tested in a plus maze. Results: This exposure led to no gross anatomical abnormalities or increased morbidity or mortality. Overall activity was not significantly affected by embryonic ethanol exposure. A trend towards a dose-dependent decrease in learning and memory performance was observed. Conclusions: We suggest that zebrafish will be an appropriate model with which one can analyze the behavioural effects of embryonic alcohol exposure and the mechanisms of the ensuing abnormalities.

Background: Fetal alcohol syndrome (FAS) is a devastating disorder whose mechanisms may be best investigated using animal models. Here we present a novel zebrafish FAS model to investigate the effects of low to moderate alcohol exposure during early development on learning. Methods: At 24-hours postfertilization zebrafish embryos were exposed to low doses of ethanol (external concentrations = 0.00, 0.25, 0.50, 0.75 and 1.00% vol/vol) for a very short duration (2 hours). Upon adulthood associative learning in the zebrafish was tested in a plus maze. Results: This exposure led to no gross anatomical abnormalities or increased morbidity or mortality. Overall activity was not significantly affected by embryonic ethanol exposure. A trend towards a dose-dependent decrease in learning and memory performance was observed. Conclusions: We suggest that zebrafish will be an appropriate model with which one can analyze the behavioural effects of embryonic alcohol exposure and the mechanisms of the ensuing abnormalities.

In 1996, the Institute of Medicine made an initial step towards addressing the confusion and controversy regarding the diagnosis of fetal alcohol syndrome (FAS) by proposing a classification scheme and calling for research to evaluate its validity and clinical utility. Previous research evaluated memory, executive functions, and behaviour problems in FAS. Prior to the present study, however, there had not been an empirical evaluation of the existence of a spectrum of diagnostic subgroups or an evaluation of subgroup functioning on neuropsychological components of attention during the pre-teen and adolescent years. Part 1 of this study used categorical data regarding diagnostic domains to determine if an a priori spectrum of four subgroups could be identified. This spectrum included FAS and three fetal alcohol effect (FAE) subgroups, which were defined using teratogenic theory, previous research findings, and logic. The sample consisted of 112 children with a confirmed history of excessive prenatal alcohol exposure. Part 2 evaluated the continuity and comparability of the CNS dysfunction subgroups exhibited by assessing neuropsychological components of attention using models by Mirsky and Conners. The sample consisted of 30 children and subgroups were matched on age, sex, and living situation. Results identified 3 of the 4 potential subgroups. All subgroups exhibited a clinically significant attention deficit. After adjusting for IQ, the FAS and FAE subgroups had comparable levels of functioning on all components of attention with one exception. On the sustain component, the FAE subgroups had more difficulties than the FAS subgroup in maintaining a consistent response-speed in response to changes in the length of time between targets. This study provides empirical and theoretical support for the validity and clinical utility of a spectrum of fetal alcohol subgroups consistent with the IOM's classification. It furthers a theoretical understanding of the dose-response effects of alcohol as a teratogenic agent. It suggests that attention regulation functions are especially vulnerable to the damage caused by prenatal alcohol exposure. The findings emphasize the importance of obtaining a history of prenatal alcohol exposure in individuals presenting with neuropsychological difficulties, and developing treatment programs for pregnant women with an alcohol addiction.

Thesis (Ph. D.)--West Virginia University, 2003. / Title from document title page. Document formatted into pages; contains vii, 146 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.

Maternal consumption of ethanol during pregnancy contributes to a set of pathologies, grouped together as the fetal alcohol spectrum disorders, affecting as many as 5% of live births in the United States annually. Ethanol acts widely in the developing embryo, affecting many tissues, but causing deficits in neuronal and neural crest populations particularly. These deleterious effects cause archetypical craniofacial expression and neurological deficits, including microcephaly and neuronal dysfunction. Severity of symptoms is linked to frequency of maternal alcohol consumption as well as the maximum blood alcohol concentration reached by the mother. The teratology of ethanol has been widely researched over the last four decades, with the link between the neural crest pathology and the fetal alcohol spectrum phenotype becoming clearer. Animal model studies have managed to replicate many of the symptoms seen in humans afflicted with fetal alcohol spectrum disorders, and have allowed us to elucidate the biochemical mechanisms behind the disease. There is no singular pathway responsible for the fetal alcohol spectrum disorders: over half a dozen models of dysfunction have been identified, and ethanol’s ability to react with a series of targets means that more pathways are likely to be discovered. Current theories regarding the effects of ethanol on the neural crest have implicated apoptosis of the cephalic neural crest, mediated by G-protein coupled receptors, activation of a phospholipase C pathway, and subsequent release of intracellular calcium; perturbations of the actin cytoskeleton leading to migration dysfunction of neural crest cells in the developing neural tube; lack of functional trophic molecules, specifically Shh, likely due to dysfunction of the cholesterol biosynthetic pathway; lack of retinoic acid production; oxidative stress, production of reactive oxygen species, and iron dysregulation; and genetics, which seems to confer greater susceptibility and resistance to ethanol in certain individuals. Ultimately, a global model for ethanol’s actions on the developing fetus eludes researchers, as do any potential treatments, and more research is required to further elucidate ethanol’s teratogenic mechanism.

Thesis (MA)--University of Stellenbosch, 2004. / ENGLISH ABSTRACT: The objective of this thesis is to review and synthesize the scientific literature on cognitive and neuropsychological deficits associated with children who were exposed to alcohol prenatally and to highlight possible areas of future attention. High incidences of Fetal Alcohol Syndrome has been reported especially in patients from low socio-economic areas. The highest reported incidence is found in the Western Cape province in South Africa. The devastating part of FAS is that its affects are entirely preventable. Alcohol is a physical and a behavioural teratogen. Prenatal alcohol exposure causes structural damage to the central nervous system and the brain that is vulnerable throughout the pregnancy. A dose-response association exist as exposure to heavier amounts of alcohol can cause more harm. The timing and pattern of alcohol consumption also plays a role. To date though, no "safe" level of alcohol consumption during pregnancy can be advocated. Various neuropsychological decrements are found in individuals with fetal alcohol syndrome or alcohol related neuro-developmental deficits as evaluated on standardized tests. Mental retardation is commonly found and even individuals with normal IQ's still display other learning disabilities. IQ's remain stable over the life span. Along with impaired intellectual functioning they also struggle with mathematical tasks especially as their complexity increases. Speech and language development is also delayed in individuals with FAS. There is little variation in the pith and display poor language comprehension. Attentional deficits are also noted and especially impact on academic functioning. Clinically, children often present with ADHD but in-depth studies have revealed that neurobiologically there is some differences as children with FAS struggle more with encoding and shifting of attention as opposed to other patients with ADHD. Difficulties with visual-spatial functioning has also been found. Verbal learning and memory are also impaired in individuals with FAS. Their poor verbal learning are influenced by their shallow level of encoding. Problems with fine motor skills are also noted. It also appear that all executive functions are impaired. They demonstrate poor planning skills, initiation, cognitive shifting, slow information processing, their thinking is concrete and they have poor self-regulatory skills. Behavioural problems include impulsivity, hyperactivity, aggressiveness, poor social skills and impaired judgement. Early intervention is thus essential to lessen the impact of neuro-psychological deficits on functional adaptation. A sensitive battery of neuro-psychological tests are also required to identify all the impairments in affected individuals and to plan more focussed intervention strategies. / AFRIKAANSE OPSOMMING: In hierdie tesis word 'n oorsig aangebied van literatuur wat betrekking het op die disfunksie van kinders wie se moeders tydens swangerskap alkohol misbruik het. Leemtes asook moontlike areas van toekomstige navorsing, is bespreek. 'n Hoe voorkoms van fetale alkohol sindroom (FAS) word gerapporteer, pasiente uit die lae SES gebiede. Die hoogste voorkoms word gerapporteer in die Wes- Kaapse provinsie in Suid Afrika. Wat die probleem meer tragies maak, is die feit dat dit heeltemal voorkombaar is. Alkohol is 'n teratogeen wat fisieke, neurologiese en gedragsimplikasies het. Blootstelling aan alkohol voor geboorte veroorsaak strukturele veranderinge in die sentrale senuweestelsel en die brein. Blootstelling tot hoer volumes van alkohol veroorsaak noodwendig meer skade. Die spesifieke stadium van alkohol-inname tydens die swangerskap, en die moeder se drinkpatroon, speel 'n rol in die neurosielkundige uitkomste. Tot op hede kon geen veilige alkoholsvlak tydens swangerskap vasgestel word nie. Verskeie neurosielkundige uitvalle is gevind in kinders met FAS en ook kinders met alkohol-verwante neurologies ontwikkelings probleme, volgens neurosielkundige toetsing. Verstandelike gestremdheid kom algemeen voor in kinders met FAS. Kinders met FAS wat oor normale intellektuele vernoens beskik ervaar leerprobleme. Die intellektuele inkortings bly stabiel oor die lewenspan. Kinders met FAS ondervind erge probleme met wiskunde, veral wanneer die werk moeiliker raak. Die spraak-en taalontwikkeling wat kinders met FAS ervaar sluit in beperkte taalbegrip en intonasie. Hulle kort aandagspan affekteer veral hulle akademiese funksionering. Die aandagsteuring van kinders met FAS en kinders met aandagstekort-hiperaktiwiteit versteuring verskil neuro-biologies. Verdere verskille bestaan ook aangesien kinders met FAS spesifiek sukkel met swak enkoderingsvermoe en om kognitiewe aanpassings te maak. Visueel-ruimtelike verrnoe van kinders met FAS is ook benadeel. Hulle sukkel ook met verbale leer en hulle geheue is ook ingekort. Die inkortings dui op 'n oppervlakkige enkoderingsvermoe. Probleme met fyn-motoriese vaardighede is ook gevind, volgens toetseing. Toetse wat gemik is om uitvoerende funksies te evalueer, het verskeie uitvalle aan die lig gebring. Probleme in abstrakte redenering, beplanning, impulsiwiteit, self-regulering, en die lnlslerlnq en prosessering van informasie. Gedragsprobleme soos swak sosialiseringsvaardighede, aggresiwiteit, swak oordeel en hiperaktiwiteit. Die wye neurosielkundige uitvalle wat voorkom in kinders met FAS noodsaak vroee intervensie om die langtermyn-impak daarvan te verminder. Hiervoor word 'n sensitiewe battery neurosielkundige toetse benodig wat al die kognitiewe uitvalle kan identifiseer.

Optimal maternal nutritional status is required for development of a healthy infant. Drinking during pregnancy puts mothers at risk for nutrient deficiencies, endangering the health of the fetus and increasing the risk of Fetal Alcohol Spectrum Disorder (FASD). The current body of research has focused on interventions using nutrients important to fetal brain development (choline, DHA, folate, vitamin A, zinc) to reduce FASD in animal models. Whether mothers at risk for having a baby with FASD are consuming adequate amounts of these nutrients during pregnancy is unknown, due to a lack of sufficient research data. Therefore, this study aims to identify intake of nutrients important to fetal brain development in pregnant mothers. Through community engagement and partnerships with Mount Carmel Clinic and other prenatal programs located in Point Douglas and Downtown Winnipeg, 56 pregnant women were recruited and interviewed. Findings show that intake of certain nutrients important to fetal brain development are not being consumed in recommended amounts. While most participants met the Dietary Reference Intakes for zinc and vitamin A, only 44.6% met recommendations for folate, 48.2% for choline, and 16.1% for DHA. Dietary intake was not significantly different between women with alcohol exposure during pregnancy and those without. These results are important due to the high rate (46%) of women with prenatal alcohol exposure. Study outcomes may provide future nutrition interventions to enhance the health of mothers consuming alcohol during pregnancy and their infants, potentially reducing the effects of FASD. / October 2016