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Prenatal Exposure (prenatal + exposure)

Distribution by Scientific Domains

Medical Sciences	50%
Life Sciences	31%
Humanities and Social Sciences	9%
3 Other Domains	10%

Selected Abstracts

The Timing of Prenatal Exposure to Maternal Cortisol and Psychosocial Stress Is Associated With Human Infant Cognitive Development

CHILD DEVELOPMENT, Issue 1 2010
Elysia P. Davis
The consequences of prenatal maternal stress for development were examined in 125 full-term infants at 3, 6, and 12 months of age. Maternal cortisol and psychological state were evaluated 5 times during pregnancy. Exposure to elevated concentrations of cortisol early in gestation was associated with a slower rate of development over the 1st year and lower mental development scores at 12 months. Elevated levels of maternal cortisol late in gestation, however, were associated with accelerated cognitive development and higher scores at 12 months. Elevated levels of maternal pregnancy-specific anxiety early in pregnancy were independently associated with lower 12-month mental development scores. These data suggest that maternal cortisol and pregnancy-specific anxiety have programming influences on the developing fetus. [source]

Disruption of brain development in male rats exposed prenatally to 5-bromo-2,-deoxyuridine

CONGENITAL ANOMALIES, Issue 4 2001
Makiko Kuwagata
ABSTRACT, Sprague-Dawley rats were treated intraperitoneally with 5-bromo-2,-deoxyuridine (BrdU) at 0,12.5 or 50 mg/kg/day on days 9 through 15 of gestation to evaluate the effects on development of the brain of offspring. Prenatal exposure to BrdU induced abnormal development of the brain; dilatation of the lateral ventricles in male offspring in the postnatal period. The ratio of the length of the longitudinal fissure to that of the cerebral cortex decreased in a dose-dependent manner in the embryonic period and thereafter. In 14-week-old male offspring exposed prenatally to BrdU at 50 mg/kg, the cortex layer of the cerebrum was thinner than that of the controls. Masculine sexual behavior was markedly impaired and the volume of the sexually dimorphic nucleus of the preoptic area (SDN-POA) was decreased in the 50 mg/kg group as compared with the controls. These results demonstrate that prenatal exposure to BrdU affected the development of the brain hi the prenatal and postnatal stages and reduced the volume of SDN-POA after puberty, resulting in a disruption of reproductive ability in male rats. [source]

Effects of alcohol and smoking during pregnancy on infant autonomic control

DEVELOPMENTAL PSYCHOBIOLOGY, Issue 3 2009
William P. Fifer
Abstract Prenatal exposure to smoking and alcohol increases the risk for Sudden Infant Death Syndrome (SIDS). Physiological changes associated with these exposures are not well studied. Full-term infants were tested within the first 3 days of life. We hypothesized that maternal alcohol consumption and/or smoking during pregnancy would alter autonomic nervous system function. Newborns whose mothers smoked during pregnancy had lower beat-to-beat heart rate variability in quiet sleep. Infants whose mothers consumed alcohol had lower global heart rate variability, but only in active sleep. Unexposed infants demonstrated increases in heart rate with head-up tilt and decreases in heart rate with head-down tilt, but smoking and alcohol-exposed infants showed no significant responses. These results indicate that autonomic function is altered by prenatal exposure to alcohol and smoking. Such markers may provide early identification of infants at greatest risk for SIDS. © 2009 Wiley Periodicals, Inc. Dev Psychobiol 51: 234,242, 2009 [source]

Transnatal olfactory continuity in the rabbit: Behavioral evidence and short-term consequence of its disruption

DEVELOPMENTAL PSYCHOBIOLOGY, Issue 4 2002
Gérard Coureaud
Abstract This study investigates the role of prenatal odor learning on postnatal adaptive orientation responses in the newborn rabbit. Preference tests revealed that pups are equally attracted to the odors of placentae and colostrum (Experiments 1,4), suggesting that an odor continuity may exist between the fetal and neonatal environments. To test some predictions derived from this hypothesis, we manipulated the odor of the diet of pregnant-lactating does to control the chemical niches of their perinates. Fetuses exposed in this way to the odor of cumin (C) were selectively attracted as neonates to the odor of pure C (Experiment 6). Prenatal exposure to C also was followed, to a certain extent, by enhanced attraction to C odor in the placenta or colostrum from females which had consumed it (Experiments 5 & 7). Finally, the functional implications of perinatal odor continuity were tested by disrupting it. The odor component of the feto,neonatal transitional environment revealed indeed to affect the ability of certain pups to gain colostrum and milk at the very first sucking opportunities (Experiment 8). © 2002 Wiley Periodicals, Inc. Dev Psychobiol 40: 372,390, 2002. Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/dev.10038 [source]

Prenatal cocaine exposure and infant sleep at 7 months of age: The influence of the caregiving environment

INFANT MENTAL HEALTH JOURNAL, Issue 4 2006
Pamela Schuetze
The primary goal of this study was to examine sleep problems in a sample of cocaine-exposed 7-month-old infants and to determine if maternal psychopathology mediated any existing association between substance exposure and sleep behaviors. We also examined the differences in sleep behaviors of cocaine-exposed infants in parental custody and cocaine-exposed infants in nonparental custody. Participants were 65 cocaine-exposed and 53 nonexposed infants and their primary caregivers who were recruited at delivery and assessed at 7 months of infant age. As expected, women who used cocaine during pregnancy had more psychiatric symptoms than nonusers. Prenatal exposure to heavier amounts of cocaine was significantly related to more severe sleep difficulties, and maternal anxiety mediated this association. Approximately 28% of cocaine mothers lost custody of their infants by 7 months of age. Nonmaternal caregivers had significantly fewer symptoms of psychopathology than the cocaine-using women who retained custody of their children. Infants who were in nonparental care at 7 months of age also had less severe sleep problems than did infants who remained in parental care. [source]

The Impact of Maternal Age on the Effects of Prenatal Alcohol Exposure on Attention

ALCOHOLISM, Issue 10 2010
Lisa M. Chiodo
Background:, Prenatal exposure to alcohol has a variety of morphologic and neurobehavioral consequences, yet more than 10% of women continue to drink during pregnancy, placing their offspring at risk for fetal alcohol spectrum disorders (FASD). Identification of at-risk pregnancies has been difficult, in part, because the presence and severity of FASD are influenced by factors beyond the pattern of alcohol consumption. Establishing maternal characteristics, such as maternal age, that increase the risk of FASD is critical for targeted pregnancy intervention. Methods:, We examined the moderating effect of maternal age on measures of attention in 462 children from a longitudinal cohort born to women with known alcohol consumption levels (absolute ounces of alcohol per day at conception) who were recruited during pregnancy. Analyses examined the impact of binge drinking, as average ounces of absolute alcohol per drinking day. Smoking and use of cocaine, marijuana, and opiates were also assessed. At 7 years of age, the children completed the Continuous Performance Test, and their teachers completed the Achenbach Teacher Report Form. Results:, After controlling for covariates, stepwise multiple regression analyses revealed a negative relation between levels of prenatal binge drinking and several measures of attention. The interaction between alcohol consumption and maternal age was also significant, indicating that the impact of maternal binge drinking during pregnancy on attention was greater among children born to older drinking mothers. Conclusion:, These findings are consistent with previous findings that children born to older alcohol-using women have more deleterious effects of prenatal alcohol exposure on other neurobehavioral outcomes. [source]

Fetal Exposure to Moderate Ethanol Doses: Heightened Operant Responsiveness Elicited by Ethanol-Related Reinforcers

ALCOHOLISM, Issue 11 2009
Samanta M. March
Background:, Prenatal exposure to moderate ethanol doses during late gestation modifies postnatal ethanol palatability and ingestion. The use of Pavlovian associative procedures has indicated that these prenatal experiences broaden the range of ethanol doses capable of supporting appetitive conditioning. Recently, a novel operant technique aimed at analyzing neonatal predisposition to gain access to ethanol has been developed. Experiment 1 tested the operant conditioning technique for developing rats described by Arias and colleagues (2007) and Bordner and colleagues (2008). In Experiment 2, we analyzed changes in the disposition to gain access to ethanol as a result of moderate prenatal exposure to the drug. Methods:, In Experiment 1, newborn pups were intraorally cannulated and placed in a supine position that allowed access to a touch-sensitive sensor. Paired pups received an intraoral administration of a given reinforcer (milk or quinine) contingent upon physical contact with the sensor. Yoked controls received similar reinforcers only when Paired pups activated the circuit. In Experiment 2, natural reinforcers (water or milk) as well as ethanol (3% or 6% v/v) or an ethanol-related reinforcer (sucrose compounded with quinine) were tested. In this experiment, pups had been exposed to water or ethanol (1 or 2 g/kg) during gestational days 17 to 20. Results:, Experiment 1 confirmed previous results showing that 1-day-old pups rapidly learn an operant task to gain access to milk, but not to gain access to a bitter tastant. Experiment 2 showed that water and milk were highly reinforcing across prenatal treatments. Furthermore, general activity during training was not affected by prenatal exposure to ethanol. Most importantly, prenatal ethanol exposure facilitated conditioning when the reinforcer was 3% v/v ethanol or a psychophysical equivalent of ethanol's gustatory properties (sucrose,quinine). Conclusions:, The present results suggest that late prenatal experience with ethanol changes the predisposition of the newborn to gain access to ethanol-related stimuli. In conjunction with prior literature, this study emphasizes the fact that intrauterine experience with ethanol not only augments ethanol's palatability and ingestion, but also facilitates the acquisition of response,stimulus associations where the drug acts as an intraoral reinforcer. [source]

Behavioral Outcomes for Substance-Exposed Adopted Children: Fourteen Years Postadoption

AMERICAN JOURNAL OF ORTHOPSYCHIATRY, Issue 1 2008
LCSW, Thomas M. Crea Ph.D.
From a life course perspective, studies of cumulative disadvantage often identify early risk factors as predictors of poor outcomes. This study examined the influence of prenatal substance exposure on children's externalizing behaviors at 14 years postadoption. Using Wave 4 data from the California Long-Range Adoption Study, the authors employed growth curve modeling to examine behavioral trajectories of 275 children as influenced by foster care status, age at adoption, and gender. Outcomes are measured using a shortened Behavioral Problem Index. Prenatal exposure predicted elevated behavior problems that increased normatively compared with nonexposed children, and were not found to trigger the negative behavior sequelae once feared. Foster children tended to fare better over the life course than those adopted through other means, except for children adopted at older ages. Adopted children's problem behaviors may be directly associated with the success of their placements. The authors discuss implications for practice and future research. [source]

Prenatal synthetic glucocorticoid exposure alters hypothalamic,pituitary,adrenal regulation and pregnancy outcomes in mature female guinea pigs

THE JOURNAL OF PHYSIOLOGY, Issue 5 2010
Elizabeth Dunn
Preterm delivery occurs in approximately 10% of all pregnancies. Prenatal exposure to synthetic glucocorticoids (sGCs) reduces the incidence of respiratory distress syndrome (RDS) in these babies. Therefore, administration of multiple courses of sGCs became common practice. Animal and human studies have demonstrated that multiple courses of sGCs can have long-term effects. While the majority of animal studies have been undertaken in male offspring, it is emerging that there are profound sex differences in the consequences of prenatal sGC exposure. To our knowledge, no studies have determined the effects of prenatal sGC exposure on hypothalamic,pituitary,adrenal (HPA) axis function in female offspring while accounting for reproductive cycle status, or determined if there are effects on pregnancy parameters. Pregnant guinea pigs were administered three courses of betamethasone (Beta), dexamethasone (Dex) or vehicle on gestational days 40/41, 50/51 and 60/61. In adulthood (age range: postnatal days 126,165), basal and activated HPA axis function were assessed at various stages of the reproductive cycle. The female offspring were then mated and underwent an undisturbed pregnancy. Females were killed in the luteal phase of the reproductive cycle following litter weaning, and molecular analysis undertaken. In the luteal phase, Beta-exposed females exhibited significantly lower basal salivary cortisol levels (P < 0.05). Dex-exposed females also exhibited significantly lower basal salivary cortisol levels during the luteal phase (P < 0.05), but increased basal salivary cortisol levels during the ostrous phase (P < 0.01). The Beta-exposed females exhibited increased glucocorticoid receptor (GR) mRNA expression in the CA1/2 region of the hippocampus (P < 0.05) and MC2R mRNA in the adrenal cortex (P < 0.05). The Dex-exposed animals exhibited higher hippocampal GR and mineralocorticoid receptor (MR) mRNA levels (P < 0.05). Beta-exposed females showed reduced fecundity (P < 0.05). In Dex-exposed females there was a lower male to female sex ratio. In conclusion, prenatal sGC exposure affects HPA axis activity, in a cycle-dependent manner, and long-term reproductive success. The clinical implications of the findings on endocrine function and pregnancy in females are profound and further follow-up is warranted in human cohorts. Furthermore, we have shown there are considerable difference in phenotypes between the Beta- and Dex-exposed females and the specific endocrine and maternal outcome is contingent on the specific sGCs administered during pregnancy. [source]

Sequential developmental changes in holoprosencephalic mouse embryos exposed to ethanol during the gastrulation period,

BIRTH DEFECTS RESEARCH, Issue 7 2007
Daisuke Higashiyama
Abstract BACKGROUND: Prenatal exposure to ethanol induces holoprosencephalic malformations in both humans and laboratory animals. However, its teratogenic window for inducing holoprosencephaly is narrow, and the teratogenic mechanism is not well understood. In the present study, we examined the morphological changes in the craniofacial structures of mouse embryos/fetuses at intervals following ethanol treatment and evaluated gene expression patterns in the embryos. METHODS: Pregnant C57BL/6J mice were given two doses of ethanol (30 mg/kg in total) on the morning (7:00 and 11:00 AM) of day 7. The fetuses were observed at E10.5 and E15.5 grossly and/or histologically. The expression of Shh and Nkx2.1 gene transcripts was examined at E8.5 by in situ hybridization. RESULTS: Gross and histological abnormalities of the brain and face were found in ethanol-exposed fetuses, and their midline structures were most frequently affected. The midline commissural fibers were often lacking in ethanol-exposed fetuses, even in those cases without external gross malformations. In situ hybridization revealed down-regulation of Shh and Nkx2.1 genes in ethanol-exposed embryos. CONCLUSIONS: The results indicate that ethanol may perturb the expression of some developmental genes at a critical stage of embryonic development and induce holoprosencephaly and other midline craniofacial malformations, including histological brain abnormalities. Birth Defects Research (Part A), 2007. © 2007 Wiley-Liss, Inc. [source]

Visually impaired children with posterior ocular malformations: pre- and neonatal data and visual functions

ACTA OPHTHALMOLOGICA, Issue 4 2003
Kristina Teär Fahnehjelm
Abstract. Aim:, To analyse pre- and neonatal data and ocular findings in children with visual impairment caused by posterior ocular malformations. Methods:, Medical records were scrutinized, dried blood spot cards were analysed for virus DNA and ophthalmological assessments were performed in 28 children with optic nerve hypoplasia (ONH) and 10 with optic/chorio-retinal coloboma. Results:, Prenatal exposure to possible teratogens was documented in 5/28, herpes simplex virus type 1 DNA was identified in the dried blood spot cards of 1/26 children and neonatal hypoglycaemia in 12/28 children with ONH. The time delay from ocular to endocrinological diagnosis and treatment was 3 years. Children with ONH and severe visual impairment had endocrinopathy more often (11/13) than ONH children with better visual functions (5/15). Prenatal exposure to teratogens or neonatal hypoglycaemia was not identified in any of the children with coloboma. Conclusion:, Neonatal hypoglycaemia was common in children with ONH. Severe visual impairment predicted endocrinopathy. Analysis of dried blood spot cards could serve as an additional diagnostic tool in children with ocular malformations. [source]

Coffee consumption during pregnancy and the risk of hyperkinetic disorder and ADHD: a prospective cohort study

ACTA PAEDIATRICA, Issue 1 2009
Karen Markussen Linnet
Abstract Aim: Based on hypotheses from experimental studies, we studied the association between intrauterine exposure to coffee and the risk of clinically verified hyperkinetic disorder and attention-deficit hyperactivity disorder (ADHD). Methods: A cohort study with prospectively collected data from the Aarhus Birth Cohort, Denmark. We included 24 068 singletons delivered between 1990 and 1998. Linkage was performed with three Danish longitudinal registers: The Danish Psychiatric Central Register, The Integrated Database for Labour Market Research and The Danish Civil Registration System. We identified 88 children with hyperkinetic disorder and ADHD. Information about coffee consumption during pregnancy was obtained at 16 weeks of gestation from self-administrated questionnaires. Potential confounding factors were evaluated using Cox regression analyses. Results: We found that intrauterine exposure to 10 or more cups of coffee per day was associated with a threefold increased risk of hyperkinetic disorder and ADHD. After adjustments for a number of confounding factors, the risk decreased and became statistically insignificant (RR 2.3, 95% CI 0.9,5.9). Conclusion: Prenatal exposure to high levels of coffee did not significantly increase the risk of clinically verified hyperkinetic disorder and ADHD in childhood. [source]

Methods for detecting interactions between genetic polymorphisms and prenatal environment exposure with a mother-child design

GENETIC EPIDEMIOLOGY, Issue 2 2010
Shuang Wang
Abstract Prenatal exposures such as polycyclic aromatic hydrocarbons and early postnatal environmental exposures are of particular concern because of the heightened susceptibility of the fetus and infant to diverse environmental pollutants. Marked inter-individual variation in response to the same level of exposure was observed in both mothers and their newborns, indicating that susceptibility might be due to genetic factors. With the mother-child pair design, existing methods developed for parent-child trio data or random sample data are either not applicable or not designed to optimally use the information. To take full advantage of this unique design, which provides partial information on genetic transmission and has both maternal and newborn outcome status collected, we developed a likelihood-based method that uses both the maternal and the newborn information together and jointly models gene-environment interactions on maternal and newborn outcomes. Through intensive simulation studies, the proposed method has demonstrated much improved power in detecting gene-environment interactions. The application on a real mother-child pair data from a study conducted in Krakow, Poland, suggested four significant gene-environment interactions after multiple comparisons adjustment. Genet. Epidemiol. 34: 125,132, 2010. © 2009 Wiley-Liss, Inc. [source]

Myocardial growth before and after birth: clinical implications,

ACTA PAEDIATRICA, Issue 2 2000
AM Rudolph
Perinatal changes in myocardial growth have recently evoked considerable interest with regard to cardiac chamber development with congenital cardiac lesions and to myocardial development in preterm infants. It is suggested that cardiac chamber development is influenced by blood flow. Experimental pulmonary stenosis in fetal lambs may induce either greatly reduced or markedly increased right ventricular volume. Ventricular enlargement appears to be associated with a large ventricular volume load resulting from tricuspid valve regurgitation. A small competent tricuspid valve is associated with reduced flow through the ventricle due to outflow obstruction and a small right ventricle. Postnatal growth of the ventricles in congenital heart disease is discussed. Increase in myocardial mass prenatally is achieved by hyperplasia, both during normal development and when myocardial mass is increased by right ventricular outflow obstruction. Postnatally, increases in myocardial mass with normal growth, as well as with ventricular outflow obstruction, are largely due to hypertrophy of myocytes. Myocardial capillary numbers do not increase in proportion with myocyte numbers in ventricular myocardium in association with outflow obstruction. The postnatal effects of these changes in congenital heart lesions are considered. Studies in fetal lambs suggest that the late gestational increase in blood cortisol concentrations is responsible for the change in the pattern of myocardial growth after birth. The concern is raised that prenatal exposure of the premature infant to glucocorticoids, administered to the mother to attempt to prevent hyaline membrane disease in the infant, may inhibit myocyte proliferation and result in a heart with fewer than normal myocytes. This would necessitate that each myocyte would have to hypertrophy abnormally to achieve a normal cardiac mass postnatally. [source]

Effects of in utero exposure to 2,2,,4,4,,5,5,-hexachlorobiphenyl (PCB 153) on somatic growth and endocrine status in rat offspring

CONGENITAL ANOMALIES, Issue 4 2008
Kenichi Kobayashi
ABSTRACT Exposure to polychlorobiphenyl (PCB) mixtures at an early stage of development has been reported to affect endocrine glands; however, little is known about the precise toxicological properties of individual PCB. The present study was undertaken to determine whether prenatal exposure to 2,2,,4,4,,5,5,-hexachlorobiphenyl (PCB 153), a di- ortho -substituted non-coplanar congener, affects postnatal development in rat offspring. Pregnant Sprague-Dawley rats (Crj: CD (SD) IGS) were given PCB 153 (0, 16, or 64 mg/kg/day) orally from gestational day (GD) 10 through GD 16, and developmental parameters in the male and female offspring were examined. We found no dose-dependent changes in body weight, body length (nose,anus length), tail length, or the weights of kidneys, testes, ovaries and uterus in offspring at 1 or 3 weeks of age. Liver weights were increased in the PCB 153,treated groups, although we observed a significant difference only in males. Anogenital distance was unaffected in the PCB 153,treated groups. We observed a significant dose-dependent decrease in the plasma concentrations of thyroxine and tri-iodothyronine, whereas those of thyroid-stimulating hormone were not significantly changed. In addition, there were no dose-dependent changes in plasma concentrations of growth hormone and insulin-like growth factor-I in any dose group. These findings suggest that prenatal exposure to PCB 153 (GD 10,16, 16,64 mg/kg/day) may alter the thyroid status in rat offspring to some extent without affecting somatic growth or its related hormonal parameters. [source]

Disruption of brain development in male rats exposed prenatally to 5-bromo-2,-deoxyuridine

Prenatal and family risks of children born to mothers with epilepsy: effects on cognitive development

DEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 2 2008
Karl Titze PhD
The offspring of mothers with epilepsy are considered to be at developmental risk during pregnancy from: (1) generalized maternal seizures (hypoxia); (2) teratogenicity of antiepileptic drugs (AEDs); and (3) adverse socio-familial conditions associated with having a chronically sick mother. Sixty-seven children of mothers with epilepsy and 49 children from non-affected mothers, matched for control variables, were followed from birth to adolescence (53 males, 63 females; mean age 14y 2mo, range 10-20y). Prediction of intellectual performance of these children during adolescence was calculated from the following variables: maternal generalized seizures, prenatal exposure to AEDs, and quality of family stimulation (HOME Inventory) assessed in children at 2 years of age. Children who were prenatally exposed to AEDs achieved lower IQs than control children at adolescence. This effect was moderately significant for children who had been exposed to monotherapy (6 IQ points lower), but was considerable in those exposed to polytherapy (12 IQ points lower). Generalized seizures during pregnancy, observed in half the mothers, did not exacerbate this effect. Relative to prenatal risk status, the quality of the family environment had varied effects on intellectual development. Children with prenatal risks appeared to be more vulnerable to environmental disadvantage than control children, but they also showed longer-lasting effects of environmental support. [source]

Brain dysmorphology in individuals with severe prenatal alcohol exposure

DEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 3 2001
Sarah L Archibald MA
Our previous studies revealed abnormalities on structural MRI (sMRI) in small groups of children exposed to alcohol prenatally. Microcephaly, disproportionately reduced basal ganglia volume, and abnormalities of the cerebellar vermis and corpus callosum were demonstrated. The present study used sMRI to examine in detail the regional pattern of brain hypoplasia resulting from prenatal exposure to alcohol using a higher resolution imaging protocol and larger sample sizes than reported previously. Fourteen participants (mean 11.4 years; eight females, six males) with fetal alcohol syndrome (FAS) and 12 participants (mean 14.8 years; four females, eight males) with prenatal exposure to alcohol (PEA) but without the facial features of FAS were compared to a group of 41 control participants (mean 12.8 years, 20 females, 21 males). Findings of significant microcephaly and disproportionately reduced basal ganglia volumes in the FAS group were confirmed. Novel findings were that in FAS participants, white matter volumes were more affected than gray matter volumes in the cerebrum, and parietal lobes were more affected than temporal and occipital lobes. Among subcortical structures, in contrast to the disproportionate effects on caudate nucleus, the hippocampus was relatively preserved in FAS participants. Differences between the PEA group and controls were generally non-significant; however, among a few of the structures most affected in FAS participants, there was some evidence for volume reduction in PEA participants as well, specifically in basal ganglia and the parietal lobe. There were no group differences in cerebral volume asymmetries. Severe prenatal alcohol exposure appears to produce a specific pattern of brain hypoplasia. [source]

Brainstem mechanisms underlying the sudden infant death syndrome: Evidence from human pathologic studies

DEVELOPMENTAL PSYCHOBIOLOGY, Issue 3 2009
Hannah C. Kinney
Abstract The brainstem hypothesis is one of the leading hypotheses concerning the sudden infant death syndrome (SIDS). It states that SIDS, or an important subset of SIDS, is due to abnormal brainstem mechanisms in the control of respiration, chemosensitivity, autonomic regulation, and/or arousal which impairs the infant's response to life-threatening, but often occurring, stressors during sleep (e.g., hypoxia, hypercarbia, asphyxia, hyperthermia) and leads to sudden death in a vulnerable developmental period. In this review, we summarize neuropathologic evidence from SIDS cases that support this hypothesis, beginning with the seminal report of subtle brainstem gliosis three decades ago. We focus upon recent neurochemical studies in our laboratory concerning the neurotransmitter serotonin (5-HT) and its key role in mediating protective responses to homeostatic stressors via medullary circuits. The possible fetal origin of brainstem defects in SIDS is reviewed, including evidence for adverse effects of prenatal exposure to maternal cigarette smoking and alcohol upon the postnatal development of human brainstem 5-HT pathways. © 2009 Wiley Periodicals, Inc. Dev Psychobiol 51: 223,233, 2009 [source]

Effects of alcohol and smoking during pregnancy on infant autonomic control

A Longitudinal Examination of Physiological Regulation in Cocaine-Exposed Infants Across the First 7 Months of Life

INFANCY, Issue 1 2009
Pamela Schuetze
This study examined the association between prenatal exposure to cocaine and physiological regulation across the first 7 months of age. Measures of respiratory sinus arrhythmia (RSA) were obtained from 169 (82 cocaine-exposed and 87 nonexposed) infants during baseline periods at 1 month and 7 months of age and during tasks designed to elicit positive and negative affect at 7 months of age. After controlling for maternal age, gestational age, and obstetrical risk, structural equation modeling indicated that the association between prenatal exposure to cocaine and baseline RSA at 7 months of age was direct even in the presence of an indirect effect through baseline RSA at 1 month of age. There were no indirect effects through maternal affect during mother-infant interactions assessed at 1 month of age. Analyses also indicated a direct association between prenatal exposure to cocaine and RSA regulation to negative affect at 7 months of age. [source]

Fetal and offspring arrhythmia following exposure to nicotine during pregnancy

JOURNAL OF APPLIED TOXICOLOGY, Issue 1 2010
Yu Feng
Abstract Although recent studies have demonstrated prenatal nicotine can increase cardiovascular risk in the offspring, it is unknown whether exposure to nicotine during pregnancy also may be a risk for development of arrhythmia in the offspring. In addition, in previous studies of fetal arrhythmia affected by smoking, only two patterns, bradycardia and tachycardia, were observed. The present study examined acute effects of maternal nicotine on the fetal arrhythmia in utero, and chronic influence on offspring arrhythmia at adult stage following prenatal exposure to nicotine. Nicotine was administered to pregnant ewes and rats. In the fetal sheep, intravenous nicotine not only induced changes of fetal heart rate, but also caused cardiac cycle irregularity, single and multiple dropped cardiac cycles. Although maternal nicotine had no influence on fetal blood pH, lactic acid, hemocrit, Na+, K+ levels and plasma osmolality, fetal blood PO2 levels were significantly decreased following maternal nicotine in ewes. In offspring rats at 4,5 months after birth, prenatal exposure to nicotine significantly increased heart rate and premature ventricular contraction in restraint stress. In addition, arrhythmias induced by injection of nicotine were higher in the offspring prenatal exposure to nicotine in utero. The results provide new evidence that exposure to nicotine in pregnancy can cause fetal arrhythmia in various patterns besides tachycardia and bradycardia, the possible mechanisms for nicotine-induced fetal arrhythmia included in utero hypoxia. Importantly, following exposure to nicotine significantly increased risk of arrhythmia in the adult offspring. The finding offers new insight for development of cardiac rhythm problems in fetal origins. Copyright © 2009 John Wiley & Sons, Ltd. [source]

Multiple Roles for the Endocannabinoid System During the Earliest Stages of Life: Pre- and Postnatal Development

JOURNAL OF NEUROENDOCRINOLOGY, Issue 2008
E. Fride
The endocannabinoid system, including its receptors (CB1 and CB2), endogenous ligands (,endocannabinoids'), synthesising and degrading enzymes, as well as transporter molecules, has been detected from the earliest stages of embryonic development and throughout pre- and postnatal development. In addition, the endocannabinoids, notably 2-arachidonyl glycerol, are also present in maternal milk. During three distinct developmental stages (i.e. embryonic implantation, prenatal brain development and postnatal suckling), the endocannabinoid system appears to play an essential role for development and survival. Thus, during early pregnancy, successful embryonic passage through the oviduct and implantation into the uterus both require critical enzymatic control of optimal anandamide levels at the appropriate times and sites. During foetal life, the cannabinoid CB1 receptor plays a major role in brain development, regulating neural progenitor differentiation into neurones and glia and guiding axonal migration and synaptogenesis. Postnatally, CB1 receptor blockade interferes with the initiation of milk suckling in mouse pups, by inducing oral motor weakness, which exposes a critical role for CB1 receptors in the initiation of milk suckling by neonates, possibly by interfering with innervation of the tongue muscles. Manipulating the endocannabinoid system by pre- and/or postnatal administration of cannabinoids or maternal marijuana consumption, has significant, yet subtle effects on the offspring. Thus, alterations in the dopamine, GABA and endocannabioid systems have been reported while enhanced drug seeking behaviour and impaired executive (prefrontal cortical) function have also been observed. The relatively mild nature of the disruptive effects of prenatal cannabinoids may be understood in the framework of the intricate timing requirements and frequently biphasic effects of the (endo)cannabinoids. In conclusion, the endocannabinoid system plays several key roles in pre- and postnatal development. Future studies should further clarify the mechanisms involved and provide a better understanding of the adverse effects of prenatal exposure, in order to design strategies for the treatment of conditions such as infertility, mental retardation and failure-to-thrive. [source]

Exposure to Oestrogen Prenatally Does Not Interfere with the Normal Female-Typical Development of Odour Preferences

JOURNAL OF NEUROENDOCRINOLOGY, Issue 5 2007
J. Bakker
The neural mechanisms controlling mate recognition and heterosexual partner preference are sexually differentiated by perinatal actions of sex steroid hormones. We previously showed that the most important action of oestrogen during prenatal development is to defeminise and, to some extent, masculinise brain and behaviour in mice. Female mice deficient in alpha-foetoprotein (AFP) due to a targeted mutation in the Afp gene (AFP-KO) do not show any female sexual behaviour when paired with an active male because they lack the protective action of AFP against maternal oestrogens. In the present study, we investigated whether odour preferences, another sexually differentiated trait in mice, are also defeminised and/or masculinised in AFP-KO females due to their prenatal exposure to oestrogens. AFP-KO females of two background strains (CD1 and C57Bl/6j) preferred to investigate male over female odours when given the choice between these two odour stimuli in a Y-maze, and thus remained very female-like in this regard. Thus, the absence of lordosis behaviour in these females cannot be explained by a reduced motivation of AFP-KO females to investigate male-derived odours. Furthermore, the presence of a strong male-directed odour preference in AFP-KO females suggests a postnatal contribution of oestrogens to the development of preferences to investigate opposite-sex odours. [source]

Verbal and Nonverbal Memory in Adults Prenatally Exposed to Alcohol

ALCOHOLISM, Issue 5 2010
Claire D. Coles
Background:, Neurocognitive effects of prenatal alcohol exposure in adulthood are not well documented. Questions persist regarding the extent to which there are specific, measurable effects beyond those associated with global ability deficits, whether individuals without the full fetal alcohol syndrome (FAS) demonstrate alcohol-related cognitive impairments, and whether observed memory effects are specific to a particular modality, i.e., verbal vs. visual/spatial domains. Methods:, In this study, verbal and nonverbal selective reminding paradigms were used to assess memory function in 234 young adults (M age: 22.78, SD: 1.79). Alcohol exposure was quantified prenatally. Alcohol groups included: Individuals with physical effects of alcohol exposure (Dysmorphic group, n = 47); Exposed individuals without such effects (n = 74). Contrast groups included: Controls (n = 59) matched for ethnicity, socioeconomic status, and hospital of birth; Special Education contrast group (n = 54) included to control for disability status. Memory outcomes entailed total recall, delayed recall, and measures of encoding and retrieval, and learning over trials as indexed by slope. Results:, Results indicated that Dysmorphic individuals were significantly less efficient in memory performance than Controls on all of the outcomes measured, but they did not differ from those in the Special Education contrast group. The nondysmorphic, alcohol-exposed group was intermediate in their performance, suggesting a continuum of effects of prenatal exposure. Evaluation of the encoding and retrieval aspects of memory performance indicated that learning rather than forgetting accounted for the deficits associated with prenatal alcohol exposure. Finally, no interaction was found between modality of presentation (verbal and nonverbal) and effects of alcohol exposure on memory performance. Conclusion:, These findings indicate that prenatal alcohol exposure is associated with persistent and specific effects on memory performance, and these problems result from less efficient encoding of information across both verbal and nonverbal modalities. Education and training efforts with this clinical group should take these characteristics into account. [source]

Fetal Exposure to Moderate Ethanol Doses: Heightened Operant Responsiveness Elicited by Ethanol-Related Reinforcers

Fatty Acid Ethyl Esters in Meconium: Are They Biomarkers of Fetal Alcohol Exposure and Effect?

ALCOHOLISM, Issue 7 2006
Enrique M. Ostrea Jr.
Background: Biomarkers of fetal exposure to alcohol are important to establish so that early detection and intervention can be made on these infants to prevent undesirable outcomes. The aim of this study was to analyze long-chain fatty acid ethyl esters (FAEEs) in meconium as potential biomarkers of fetal alcohol exposure and effect. Methods: Fatty acid ethyl esters were analyzed in the meconium of 124 singleton infants by positive chemical ionization gas chromatography/mass spectrometry (GC/MS) and correlated to maternal ethanol use. Results: A total of 124 mother/infant dyads were enrolled in the study: 31 were in the control group and 93 were in the alcohol-exposed group. The incidence (28% vs 9.7%, p=0.037) of ethyl linoleate detected in meconium was significantly higher in the alcohol-exposed groups than the control groups. Similarly, when the concentrations of ethyl linoleate in meconium were grouped (trichotomized), there was a significant linear by linear association between alcohol exposure and group concentrations of ethyl linoleate (p=0.013). Furthermore, only alcohol-exposed infants were found in the group with the highest ethyl linoleate concentration. The sensitivity of ethyl linoleate in detecting prenatal alcohol exposure was only 26.9%, and its specificity and positive predictive value were 96.8 and 96.2%, respectively. There was no significant correlation between the concentration of ethyl linoleate in meconium and absolute alcohol consumed (oz) per drinking day across pregnancy, although a trend toward a positive correlation is seen at lower amounts of alcohol consumed. Among the polyunsaturated, long-chain FAEEs, there was weak evidence that the incidence (21.5% vs 6.5%, p=0.057) and concentration (p=0.064) of ethyl arachidonate (AA) were significantly higher in the alcohol-exposed groups than the control groups. Ethyl linolenate and ethyl docosahexanoate (DHA) in meconium were found only in the alcohol group, although not at statistically significant levels. Highly significant correlations were found among the concentrations of ethyl linoleate, ethyl linolenate, ethyl AA, and ethyl DHA in meconium (correlations ranged between rs=0.203, p=0.024; and rs=0.594, p<0.001). Conclusion: We conclude that FAEEs in meconium, particularly ethyl linoleate and ethyl AA, are biomarkers of high specificity for prenatal exposure to alcohol in newborn infants. We also propose that ethyl AA and DHA could be potential biomarkers of fetal alcohol effects on the developing fetal brain and should be investigated further. [source]

Fetal Alcohol Spectrum Disorders in Children Residing in Russian Orphanages: A Phenotypic Survey

ALCOHOLISM, Issue 3 2006
Laurie C. Miller
Background: Alcohol use in Russia is among the highest in the world. Over 600,000 children reside in institutional care in Russia, most of them in baby homes and orphanages. The actual prevalence of fetal alcohol spectrum disorders (FASD) among these children is unknown. Therefore, we performed a systematic survey of phenotypic features associated with prenatal alcohol exposure among institutionalized Russian children and related these findings to their growth, development, medical, and social histories. Methods: Phenotypic screening was conducted of all 234 baby home residents in the Murmansk region of Russia (mean age 21+12.6 months). Phenotypic expression scores were devised based on facial dysmorphology and other readily observable physical findings. Growth measurements from birth, time of placement in the baby home, and at present were analyzed. In addition, the charts of 64% of the children were randomly selected for retrospective review. Information collected included maternal, medical, developmental, and social histories. Results: Thirteen percent of children had facial phenotype scores highly compatible with prenatal alcohol exposure and 45% had intermediate facial phenotype scores. These scores correlated with maternal gravidity and age. At least 40% of mothers in whom history was available ingested alcohol during pregnancy; some also used illicit drugs and tobacco. Z scores for growth measurements corresponded to phenotypic score, as did the degree of developmental delay. Children with no or mild delay had significantly lower phenotypic scores than those with moderate or severe delay (p=0.04); more than 70% of children with high phenotypic scores were moderately or severely delayed. Conclusions: More than half of residents of the baby homes in Murmansk, Russia, have intermediate (45%) or high (13%) phenotypic expression scores suggesting prenatal exposure to alcohol. Despite good physical care, stable daily routine, availability of well-trained specialists, and access to medical care, these vulnerable children show significant growth and developmental delays compared with their institutionalized peers. [source]

Fetal Alcohol Spectrum,The Hidden Epidemic in Our Courts

JUVENILE AND FAMILY COURT JOURNAL, Issue 4 2001
KATHRYN PAGE PH.D.
ABSTRACT This article discusses the basics of Fetal Alcohol Syndrome and Fetal Alcohol Effects (FAS/E): the history, nature, prevalence, causes, and effects of prenatal exposure to alcohol. Some of the unique features of FAS/E are explored, particularly those that make it so hard to spot and those that predispose people to nonproductive or criminal activity. The presentation of FAS/E in Juvenile Court is discussed and put in the context of the multiplicity of factors pertaining to delinquency; finally, innovative interventions, approaches and resources are laid out. Issues surrounding FAS/E as they appear in Family Court are then explored, with emphasis on the intergenerational transmission of this array of conditions and how we might interrupt such transmission. [source]

Craniofacial skeletal deviations following in utero exposure to the anticonvulsant phenytoin: monotherapy and polytherapy

ORTHODONTICS & CRANIOFACIAL RESEARCH, Issue 1 2003
HI Orup Jr
Structured Abstract Authors , Orup Jr HI, Holmes LB, Keith DA, Coull BA. Objective , To identify and quantify the craniofacial effects from prenatal exposure to phenytoin monotherapy and polytherapy using cephalometric, hand-wrist, and panoramic radiographs and to determine if such deviations persist with age. Design , Craniofacial structures of 28 anticonvulsant-exposed individuals were evaluated using 20 landmarks in lateral cephalometric radiographs and 19 landmarks in frontal cephalometric radiographs. Skeletal maturity was assessed using hand-wrist radiographs. Dental maturity and the presence of dental anomalies were evaluated using panoramic radiographs. Eleven individuals were re-evaluated 7 years later, on average, to determine the persistence of any measured deviations. Setting and Sample Population , Department of Growth and Development, Harvard School of Dental Medicine and Massachusetts General Hospital. Patients were recruited from several sources. Outcome Measure , The evaluated dimensions included linear, angular, and proportional measures. Results , The most common deviations were decreased height and length of the maxilla, decreased length of the posterior cranial base, length of the mandible, cranial width and level of the cribriform plate, and a decrease in the Wits Appraisal assessment. The deviations were more significant in the polytherapy-exposed individuals than in the monotherapy-exposed individuals. These deviations, especially in the maxilla, persisted with age as revealed in a re-evaluation of 11 individuals. Conclusion , The craniofacial skeletal findings among individuals exposed in utero to phenytoin monotherapy or phenytoin polytherapy, when considered in aggregate, suggest a mild pattern of maxillary hypoplasia that becomes more pronounced with age. [source]