A Longitudinal Analysis of the Effect of Prenatal Alcohol Exposure on Growth

Cross-sectional analyses have demonstrated that prenatal exposure to alcohol can result in growth deficits at birth and in early childhood. However, there have been few longitudinal analyses of this relationship. This study presents an analysis of the longitudinal effect of prenatal alcohol exposure on growth. The model used for analysis was a general unbalanced repeated-measures model with a fully parameterized covariance matrix. Application of the model demonstrated that for length and head circumference, the effect of prenatal alcohol exposure was constant over time. The relationship between prenatal alcohol exposure and growth in weight was more complex. Prenatal alcohol exposure affected the rate of growth between birth and the eighth month. Subsequently, the relationship between weight and prenatal alcohol exposure was constant Therefore, for length and head circumference, prenatal alcohol exposure suppresses the rate of growth in the fetus but not at subsequent time points. For weight, exposure affects the rate of growth through the eighth month but not at subsequent time points. For each of the growth parameters, there is no catch-up growth, and the smaller size observed in the offspring is maintained.     

Effects of Prenatal Exposure to Alcohol, Smoking, and Illicit Drugs on Postpartum Somatic Growth

The association of fetal growth retardation with prenatal exposure to alcohol, smoking, opiates, and cocaine is well documented, but relatively little is known about the effects of these exposures on postpartum growth. This study assessed physical growth from birth through 6.5 and 13 months in 412 black, inner-city infants recruited on the basis of their mothers' use of alcohol and/or cocaine during pregnancy. Prenatal alcohol exposure was associated with a slower rate of growth during the first 6.5 postpartum months. This postnatal growth retardation was associated with maternal drinking during a critical period–the latter part of gestation–and was not related to drinking at the time of conception or to postnatal exposure to alcohol from breast-feeding. By contrast, smoking and cocaine use during pregnancy were associated with faster postnatal weight gain. Although maternal smoking was correlated with shorter stature at 6.5 and 13 months, this effect was attributable to maternal drinking during pregnancy, suggesting that the association of maternal smoking with shorter childhood stature reported elsewhere may be due to prenatal alcohol exposure, which was not controlled in prior studies.     

Neuromuscular Responses to Disturbance of Balance in Children with Prenatal Exposure to Alcohol

Alcohol-exposed children display delayed motor development and impaired fine- and gross-motor skills, including deficits in the maintenance of balance. In a recent study, we assessed the contribution of visual, somatosensory, and vestibular information to the ability to maintain balance. Our findings suggested that alcohol-exposed children were overly reliant on somatosensory information and were unable to compensate by using the visual and/or vestibular systems. To understand the nature of these observed balance deficits, corrective postural reactions were examined by exposing standing subjects to rapid toe-up movements of the support surface. Subjects for this study were alcohol-exposed (ALC) and normal control (NC) children matched for age and sex. Postural reactions were quantified by measuring electromyographic activity of the triceps surae and anterior tibialis muscles. Analyses revealed no differences between the ALC and NC groups on short- and medium-latency electromyographic responses, which are thought to be involuntary mono- and polysynaptic spinal reflexes, respectively. However, when compared with the NC group, the ALC group displayed increased long-latency responses, which are thought to involve a transcortical pathway. Although we are not able to rule out the possibility of additional peripheral (e.g., vestibular) disturbance as a contributing factor to postural instability, our findings suggest that the balance deficits seen in alcohol-exposed children are, at least in part, central in nature.     

Bone Age and Growth in Fetal Alcohol Syndrome

We have found delayed mean bone age in 63 children with fetal alcohol syndrome (FAS). The mean bone age Z-score for boys ( n = 31) was −2.12 SDs and for girls ( n = 32) was -1.62 SDs. This might suggest that they have potential for catch-up growth. However, experience with children with intrauterine growth retardation suggests that this will not be the case and that FAS children will be of reduced height at maturity. Further support for this assumption was gained from a sample of 26 patients who were followed until at least the age of 14 years for females and 16 years for males. There was no significant change in height Z-scores from early childhood to early adulthood, the mean score being -2.16 SDs and -2.11 SDs at mean ages of 4.83 years and 18.69 years, respectively. On the other hand, there were significant changes in weight and head circumference. The mean weight Z-score changed from -2.10 SDs to -1.14 SDs ( p < 0.001). The head circumference mean Z-score in 16 patients was -3.13 SDs at a mean age of 2.79 years and -2.63 SDs at a mean age of 17.37 years ( p = 0.013). Short stature can continue to be used as a diagnostic criterion for FAS beyond childhood.     

Applying a Developmental Framework to the Self‐Regulatory Difficulties of Young Children with Prenatal Alcohol Exposure: A Review

Prenatal alcohol exposure (PAE) can be associated with significant difficulties in self‐regulatory abilities. As such, interventions have been developed that focus on improving varying aspects of self‐regulation for this population. The application of a multilevel theoretical framework that describes the development of self‐regulation during early childhood could further advance the field. First, this framework could assist in elucidating mechanisms in the trajectories of early adjustment problems in this population and, second, informing the development of more precise assessment and interventions for those affected by PAE. The aims of the current review were to provide an overview of the self‐regulatory framework proposed by Calkins and colleagues (e.g., Calkins, 2007; Calkins and Fox, 2002); examine the self‐regulatory difficulties that are commonly experienced during infancy (i.e., 0 to 2 years) and early childhood (i.e., 3 to 8 years) in children with PAE in the context of the developmental framework; and describe how the framework can inform the development of future assessment and intervention provision for young children with PAE. The application of a developmental framework, such as proposed by Calkins and colleagues, allows for a systematic and theoretically driven approach to assessment and intervention programs for young children with PAE.     

Prenatal Exposure to Alcohol Affects the Ability to Maintain Postural Balance

Prenatal exposure to alcohol is known to affect gross motor functioning. Animal studies have shown that balance is particularly affected, and there is some evidence that similar deficits exist in alcohol-exposed children. In the current study, postural balance, or the ability to maintain equilibrium, was assessed in a group of alcohol-exposed children (ALC group; n =11) and controls (NC group; n = 11) individually matched for age and sex. Balance was measured across six conditions designed to systematically manipulate or eliminate visual or somatosensory information. Equilibrium and strategy scores for each condition and a derived composite balance score were analyzed. Although the ALC group had a lower mean composite balance score, their performance was similar to that of the NC group on all conditions where somatosensory input was reliable. However, when somatosensory input was manipulated, and when both somatosensory and visual input were inaccurate, the ALC group performed more poorly than controls. Interestingly, there were no differences between the ALC group and NC group in the type of control strategy used to maintain balance. These results suggest that alcohol-exposed children are overly reliant on somatosensory input. When this input is atypical, alcohol-exposed children display significantly greater anterior-posterior body sway and are unable to compensate using available visual or vestibular information. These deficits may be related to cerebellar anomalies previously reported in fetal alcohol syndrome children.     

Biomarkers for the Detection of Prenatal Alcohol Exposure: A Review

Alcohol exposure during pregnancy can cause adverse effects to the fetus, because it interferes with fetal development, leading to later physical and mental impairment. The most common clinical tool to determine fetal alcohol exposure is maternal self‐reporting. However, a more objective and useful method is based on the use of biomarkers in biological specimens alone or in combination with maternal self‐reporting. This review reports on clinically relevant biomarkers for detection of prenatal alcohol exposure (PAE). A systematic search was performed to ensure a proper overview in existing literature. Studies were selected to give an overview on clinically relevant neonatal and maternal biomarkers. The direct biomarkers fatty acid ethyl esters (FAEEs), ethyl glucuronide (EtG), ethyl sulfate, and phosphatidylethanol (PEth) were found to be the most appropriate biomarkers in relation to detection of PAE. To review each biomarker in a clinical context, we have compared the advantages and disadvantages of each biomarker, in relation to its window of detectability, ease of collection, and the ease and cost of analysis of each biomarker. The biomarkers PEth, FAEEs, and EtG were found to be applicable for detection of even low levels of alcohol exposure. Meconium is an accessible matrix for determination of FAEEs and EtG, and blood an accessible matrix for determination of PEth.     

Fetal Alcohol Spectrum Disorders: A Review of the Neurobehavioral Deficits Associated With Prenatal Alcohol Exposure

In utero alcohol exposure can disrupt the development of the fetal brain and result in a wide range of neurobehavioral outcomes collectively known as fetal alcohol spectrum disorders (FASD). This paper provides a comprehensive review of the cognitive and behavioral outcomes of prenatal alcohol exposure, including domains of general intelligence, executive functioning, language development, learning and memory, adaptive functioning, academic performance, and concurrent psychopathology. In addition, the current status of the neurobehavioral profile of FASD and its potential as a diagnostic tool will be discussed.     

Sleep in Infants and Children with Prenatal Alcohol Exposure

Prenatal exposure to alcohol can result in a range of neurobehavioral impairments and physical abnormalities. The term “fetal alcohol spectrum disorders (FASD)” encompasses the outcomes of prenatal alcohol exposure (PAE), the most severe of which is fetal alcohol syndrome. These effects have lifelong consequences, placing a significant burden on affected individuals, caregivers, and communities. Caregivers of affected children often report that their child has sleep problems, and many symptoms of sleep deprivation overlap with the cognitive and behavioral deficits characteristic of FASD. Alcohol‐exposed infants and children demonstrate poor sleep quality based on measures of electroencephalography, actigraphy, and questionnaires. These sleep studies indicate a common theme of disrupted sleep pattern, more frequent awakenings, and reduced total sleep time. However, relatively little is known about circadian rhythm disruption and the neurobehavioral correlates of sleep disturbance in individuals with PAE. Furthermore, there is limited information available to healthcare providers about identification and treatment of sleep disorders in patients with FASD. This review consolidates the findings from studies of infant and pediatric sleep in this population, providing an overview of typical sleep characteristics, neurobehavioral correlates of sleep disruption, and potential avenues for intervention in the context of PAE.     

A Review of the Neuroanatomical Findings in Children with Fetal Alcohol Syndrome or Prenatal Exposure to Alcohol

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 callo-sum, 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.