This study examined the relative risk of perinatal complications in common childhood disorders. Specifically, the ability of perinatal complications to predict membership into children's disorders was studied. The sample consisted of 634 normal children and children with mental retardation, learning disabilities, and emotional handicaps, whose mothers completed the Maternal Perinatal Scale (WS). Seven MPS items significantly contributed to the prediction of the mentally retarded, learning disabled, emotionally handicapped, and regular education groups. The two significant discriminant functions correctly classified about 46% of the students, with the greatest misclassification occuring for those with emotional handicaps. When the separate disorders were collapsed to form a single group, eleven MPS items significantly contributed to the prediction of the special education and regular education groups. The linear composite from discriminant function analysis correctly classified about 74% of the students. Some 89% of the special education students were correctly classified. When MPS factors were used as predictors, 90% of the special education students were correctly classified. Seven MPS factors comprised the discriminant function. Relative risk ratios were computed for each perinatal item. Significant relative risk ratios included maternal weight over 151 pounds, saddle block anesthesia, no anesthesia, stress during pregnancy, prenatal care, medically induced labor, unplanned pregnancy, medication use during pregnancy, hypoxia, and cigarette use during pregnancy. An overall relative risk of 6.35 was computed based on the linear composite of perinatal variables defined by the discriminant function, suggesting that a suggesting that a synergism of perinatal complications makes a child over 6 times more likely to be placed in special education. A second overall relative risk of 3.83 was derived from the linear composite of MPS factor scores. This indicated that children with a perinatal history marked by this particular combination of perinatal complications were nearly 4 times as likely to require special educational services. Results were discussed in terms of comorbidity among special education categories. The potential use of the MPS as a screener for early intervention was also discussed. / Department of Educational Psychology

Thesis (M.S.)--University of Michigan, 1943.

Thesis (MA (Psychology))--University of Stellenbosch, 2010. / ENGLISH ABSTRACT: The purpose of this study was to determine the prevalence of antenatal distress in Cape Town periurban settlements, and the social factors associated with it in this population. Participants were 756 pregnant women from Khayelitsha and Mfuleni, Cape Town. Each women was interviewed in her home language using a structured questionnaire which included the Edinburgh Postnatal Depression Scale (EPDS), measures for social support and alcohol use, and questions concerning socio-demographics, intimate partner violence, and the current pregnancy. A threshold score of 14 and above on the EPDS was used to determine antenatal distress. Data were analysed using descriptive statistics and bivariate analysis initially, followed by multivariate logistical regression. Results indicated a prevalence of 46% for antenatal distress, which is substantially greater than the prevalence found in high income countries. Women in their first trimester of pregnancy were more likely to experience antenatal distress than were women in their second and third trimesters. The strongest predictors of antenatal distress were poor partner support, intimate partner violence and having a household income below R2000 per month. The high prevalence found in this study has harmful implications for infant health in South Africa, and is reason to suggest that early screening and intervention is crucial. More research is needed to develop and evaluate the effectiveness and scalability of community-based interventions for maternal depression in South African peri-urban settlements, as well as to establish the specific infant outcomes of antenatal distress in this population. / AFRIKAANSE OPSOMMING: Hierdie studie het ten doel om die voorkoms van voorgeboorteangs in buitestedelike nedersettings in Kaapstad te bepaal, sowel as die maatskaplike faktore wat met voorgeboorteangs by dié populasie verband hou. Die studiedeelnemers was 756 swanger vroue van Khayelitsha en Mfuleni, Kaapstad. ʼn Gestruktureerde vraelys is gebruik om met elke vrou ʼn onderhoud in haar huistaal te voer. Die vraelys het die Edinburg-nageboortedepressieskaal (EPDS), maatstawwe vir maatskaplike steun en alkoholgebruik, en vrae oor sosiodemografie, bedmaatgeweld en die vrou se huidige swangerskap ingesluit. ʼn Drempeltelling van 14 en hoër op die EPDS is gebruik om voorgeboorteangs te bepaal. Die data is aanvanklik met behulp van beskrywende statistiek en tweeveranderlike analise ontleed, waarna dit aan meerveranderlike logistiese regressie onderwerp is. Studieresultate toon ʼn 46%-voorkoms van voorgeboorteangs, wat beduidend hoër is as dié in hoëinkomstelande. Vroue in hul eerste trimester van swangerskap blyk meer geneig te wees om voorgeboorteangs te ervaar as vroue in hul tweede en derde trimester. Die sterkste voorspellers van voorgeboorteangs is swak ondersteuning van lewensmaats, bedmaatgeweld en ʼn huishoudelike inkomste onder R2 000 per maand. Die hoë voorkomssyfer van voorgeboorteangs waarop die studie dui, het nadelige implikasies vir babagesondheid in Suid-Afrika, en maak vroeë toetsing en ingryping noodsaaklik. Verdere navorsing word vereis om die doeltreffendheid en skaleerbaarheid van gemeenskapsgegronde ingrypings vir moederdepressie in Suid-Afrikaanse buitestedelike nedersettings te ontwikkel en te beoordeel, sowel as om die bepaalde uitwerkings van voorgeboorteangs op pasgeborenes in dié populasie te bepaal

Thesis (Ph. D.)--West Virginia University, 1999. / Title from document title page. Document formatted into pages; contains xiv, 223 p. : ill. Vita. Includes abstract. Includes bibliographical references (p. 187-220).

The intent of this research project was to discover the barriers that exist in this community when a woman attempts to access prenatal care. A concern for the well being of the children in the community and a belief in the importance of early intervention to enhance outcomes inspired the idea for this project.

Despite evidence of an association between prenatal acetaminophen exposure and attention deficit hyperactivity disorder (ADHD) in offspring, the causal role of prenatal acetaminophen exposure in child ADHD remains unclear owing to limitations of prior studies. Prior studies have relied on maternal self-report, failed to quantify acetaminophen dose, and lacked mechanistic insight. Chapter 1 formally introduces this topic and provides background information summarizing the high prevalence of ADHD, widespread use of acetaminophen during pregnancy, and potential molecular mechanisms through which the drug may harm fetal development. In Chapter 2, we examined the association between prenatal acetaminophen exposure measured in meconium and ADHD in children aged 6 to 7 years, along with the potential for mediation by functional brain connectivity. Data came from a prospective birth cohort study from the Centre Hospitalier Université de Sherbrooke in Sherbrooke, Québec, Canada. We included 393 eligible children, of whom 345 had meconium samples collected at delivery and information on ADHD diagnosis. Mothers were enrolled from September 25, 2007, to September 10, 2009, at their first prenatal care visit or delivery. Acetaminophen levels were measured in meconium, and physician diagnosis of ADHD was determined at follow-up when children were aged 6 to 7 years or from medical records. Additionally, when children were aged 9 to 11 years, resting-state brain connectivity was assessed with magnetic resonance imaging, and attention problems and hyperactivity were assessed with the Behavioral Assessment System for Children Parent Report Scale. Associations between meconium acetaminophen levels and outcomes were estimated with linear and logistic regressions weighted on the inverse probability of treatment to account for potential confounders. Causal mediation analysis was used to test for mediation of the association between prenatal acetaminophen exposure and hyperactivity by resting-state brain connectivity. Among the 345 children included in the analysis (177 boys [51.3%]; mean [SD] age, 6.58 [0.54] years), acetaminophen was detected in 199 meconium samples (57.7%), and ADHD was diagnosed in 33 children (9.6%). Compared with no acetaminophen, detection of acetaminophen in meconium was associated with increased odds of ADHD (odds ratio [OR], 2.43; 95%CI, 1.41-4.21). A dose-response association was detected; each doubling of exposure increased the odds of ADHD by 10% (OR, 1.10; 95%CI, 1.02-1.19). Children with acetaminophen detected in meconium showed increased negative connectivity between frontoparietal and default mode network nodes to clusters in the sensorimotor cortices, which mediated an indirect effect on increased child hyperactivity (14%; 95%CI, 1%-26%). In Chapter 3, we used data from the same Canadian birth cohort to examine whether prenatal acetaminophen exposure is associated with adverse birth outcomes and/or pregnancy complications, and if birth outcomes may mediate the association of prenatal acetaminophen with child ADHD. This study included 393 children for whom acetaminophen was measured in meconium at delivery. We tested associations of prenatal acetaminophen with birthweight, preterm birth, gestational age, small and large for gestational age, gestational diabetes, preeclampsia, and high blood pressure. Using causal mediation analyses, we assessed whether birth outcomes mediated the association of prenatal acetaminophen with ADHD. We imputed missing data via multiple imputation and used inverse probability weighting to account for confounding and selection bias. Prenatal acetaminophen exposure was associated with decreased birthweight by 136 g (β = −136; 95% CI [−229, −43]), 20% increased weekly hazard of delivery (hazard ratio = 1.20; 95% CI [1.00, 1.43]), and over 60% decreased odds of being born large for gestational age (odds ratio = 0.38; 95% CI [0.20, 0.75]). Prenatal acetaminophen was not associated with small for gestational age, preterm birth, or any pregnancy complications. Causal mediation effects were non-significant for all birth outcomes in both unadjusted and adjusted models, indicating no evidence that birth outcomes linked prenatal acetaminophen exposure with child ADHD. In Chapter 4, we examined the effects of developmental acetaminophen exposure on mouse behavior and frontal cortex gene expression. Although prior studies have investigated neurodevelopmental effects of prenatal acetaminophen exposure in rodents, the results of these studies are not always in agreement. Additionally, no mouse studies of prenatal acetaminophen exposure have investigated offspring attention deficits in behavior tasks specifically designed to measure attention, and no prior rodent studies have utilized ‘omics’ technologies for an untargeted exploration of potential mechanisms. We randomly assigned pregnant mice (starting embryonic day 4-10) to receive acetaminophen (150 mg/kg/day) or vehicle control through postnatal day 14. We employed a battery of behavior tests for 111 mouse offspring, including pup ultrasonic vocalizations, elevated plus maze, open field test, CatWalk, pre-pulse inhibition, and 5-choice serial reaction time task. Frontal cortex was collected at birth from 24 pups for RNA-sequencing. Developmental acetaminophen treatment resulted in increased pup vocalizations after separation from the litter, as well as decreased ambulation and vertical rearings in the open field task among male but not female offspring. Acetaminophen treatment was also associated with altered frontal cortex gene expression relating to glutathione and cytochrome p450 metabolism, DNA damage, and the endocrine and immune systems. Together with the multitude of other cohort studies showing adverse neurodevelopment associated with prenatal acetaminophen exposure, this work suggests caution should be used in administering acetaminophen during pregnancy. In humans, we found that prenatal acetaminophen exposure was associated with child ADHD, altered resting-state brain connectivity, and adverse birth outcomes. Furthermore, our results suggest altered brain connectivity as a potential underlying mechanism linking prenatal acetaminophen use with child hyperactivity. While adverse birth outcomes such as preterm birth and reduced birthweight are known to be associated with ADHD, we found no evidence for mediation by birth outcomes of the association between prenatal acetaminophen exposure and ADHD. In mice, we found that developmental acetaminophen treatment resulted in elevated anxiety-like behaviors in male offspring, as well as gene expression changes in the frontal cortex. Future studies are needed to explore whether the altered molecular pathways revealed by RNA-sequencing directly link acetaminophen exposure with offspring behavior changes.

[Truncated abstract] Glucocorticoids are critical for the maturation of the fetus late in pregnancy. Indeed, clinical administration of glucocorticoids is used to accelerate fetal lung maturation in mothers at risk of pre-term delivery. Increased glucocorticoid exposure, however, can have detrimental effects on fetal and placental growth and increase the risk of disease in later life. Many studies have focused on the effect of an increase in the transplacental passage of glucocorticoids on both fetal growth and subsequent postnatal development. But there is a growing body of evidence to suggest that the impact of glucocorticoids on fetal growth is mediated, in part, via their direct effects on the placenta . . . Overall, these studies quantify the labyrinth zone-specific increases in placental expression of PPARG and VEGF in association with a marked increase in vascularisation observed near term. Furthermore, this study demonstrates for the first time that these increases in gene expression are prevented by maternal dexamethasone treatment which also inhibits growth of the fetal capillary network. Elevated expression of SFRP4 in the regressing basal zone late in gestation and in both placental zones after dexamethasone-induced placental growth restriction is consistent with a role for SFRP4 in glucocorticoid-mediated inhibition of wnt signalling. Collectively, the data presented in this thesis show that glucocorticoid inhibition of fetal growth is mediated in large part via effects on the placenta, specifically through inhibition of signals that promote proliferation and vascularisation.