Fetal Alcohol Syndrome Children Research Articles

HEARING DISORDERS – PART OF FETAL ALCOHOL SYNDROME

Fetal alcohol syndrome (FAS) (1-2/1000 newborns), resulting from maternal consumption of alcohol early in the pregnancy, consists in: persistent growth failure, low weight, microcephaly, characteristic facial features, congenital heart diseases (especially septal defects), minor anomalies of joints and limbs, disorders of central nervous system development and function. The complexity, severity and frequency of the anomalies depends on the amount of the ingested alcohol associated or not with other risk factors: low socio-economic level, psychologic disturbances, smoking, drugs. Hearing disorders determined by maternal alcohol consumption, although not classically included in the FAS, and also chronic ear infections, are associated in variable severity degrees. Audiologic procedures performed in FAS children revealed four main hearing disorders: delayed development of auditory function associated with language disorders, sensorineural hearing loss (disorders of middle ear and conductive system), intermittent loss of sound vibrations conduction, hearing loss by central auditory nervous system deficits. Early detection of hearing anomalies alleviates the prognosis by early interventions.

Acoustic Characteristics of Stop Consonants in Children with Fetal Alcohol Syndrome

Speech of children with fetal alcohol syndrome (FAS) has been little studied compared to language. Becker, Warr-Leeper, and Leeper (1990), found a relationship between prenatal alcohol exposure, oral motor control, and speech articulation. Behavioral tests suggest deficits in focal oral motor control specific to children with FAS (Bolinger & Dembowski, 2010). The current project extends that investigation through acoustic measures. Peak and mean frequencies of stop consonant releases were used to infer control of place of articulation. Voice onset time (VOT) was used to infer articulatory-laryngeal coordination. Preliminary measures on 3 experimental speakers and 2 matched neurotypical controls suggest higher stop consonant frequencies in the experimental group, with a poorer distinction between alveolar and velar stops than in the control group. Voiced VOT values were significantly longer for FAS children than for controls. Mean voiceless VOTs were similar across groups, but substantially more variable for the FAS children. Values may be interpreted as acoustic evidence for specific speech motor control deficits in FAS children relative to matched neurotypical children.

Ethanol neurotoxicity and dentate gyrus development

Maternal alcohol ingestion during pregnancy adversely affects the developing fetus, often leading to fetal alcohol syndrome (FAS). One of the most severe consequences of FAS is brain damage that is manifested as cognitive, learning, and behavioral deficits. The hippocampus plays a crucial role in such abilities; it is also known as one of the brain regions most vulnerable to ethanol-induced neurotoxicity. Our recent studies using morphometric techniques have further shown that ethanol neurotoxicity appears to affect the development of the dentate gyrus in a region-specific manner; it was found that early postnatal ethanol exposure causes a transitory deficit in the hilus volume of the dentate gyrus. It is strongly speculated that such structural modifications, even transitory ones, appear to result in developmental abnormalities in the brain circuitry and lead to the learning disabilities observed in FAS children. Based on reports on possible factors deciding ethanol neurotoxicity to the brain, we review developmental neurotoxicity to the dentate gyrus of the hippocampal formation.

Letter and Category Fluency in Children With Fetal Alcohol Syndrome From a Community in South Africa

This study investigated whether there were differential effects of substantial prenatal alcohol exposure on letter and category fluency in children. Given that children with prenatal alcohol exposure are often impaired in executive functioning and that letter fluency taxes executive processes more than category fluency, it was expected that children with fetal alcohol syndrome (FAS) would be more impaired in letter than in category fluency. A second objective of the study was to examine the developmental trends in the two types of fluency in children with prenatal alcohol exposure. It was hypothesized that between the ages of 6 and 9 years, these FAS children would show age-related changes in category fluency but not in letter fluency. As part of a neuropsychological test battery designed for an international collaborative study of FAS in South Africa, tests of letter and category fluency were administered in Afrikaans. The participants were 62 children with FAS and 61 controls matched with respect to age, gender (58 boys and 65 girls), ethnicity, and socioeconomic status. Results showed that the FAS group had relatively greater difficulty with letter fluency than with category fluency and that the FAS group generated fewer words in both fluency conditions. Contrary to the expectation, however, alcohol-affected children demonstrated age-related linear trends in both letter and category fluency. This is the first study of verbal fluency involving a large sample of well-diagnosed children with FAS conducted in a nonwestern environment. The results are nonetheless consistent with those obtained in western countries in studies of children with various levels of prenatal alcohol exposure and various levels of fetal alcohol spectrum disorder. This study suggests that at least some aspects of the cognitive profile associated with prenatal alcohol exposure may be generalizable across cultural and ethnic boundaries.

Fetal alcohol exposure and temporal vulnerability: effects of binge-like alcohol exposure on the developing rat hippocampus

Children with fetal alcohol syndrome (FAS) display altered performance in tasks of learning and memory, behaviours thought to be associated with the hippocampus. Altered hippocampal structure has been reported in some FAS children; therefore, a rat model system was used to determine whether the size and numbers of pyramidal cells in regions CA1 and CA3 of the hippocampal formation and granule cells in the dentate gyrus were altered by alcohol exposure during different periods of development. Rat pups were exposed to alcohol in utero during the second trimester-equivalent (E10–20), the first two trimesters-equivalent (E1–20), during the time of hippocampal pyramidal cell neurogenesis (E16–20), part of the third trimester-equivalent (P4–9), and all three trimesters-equivalent (E1–20+P4–9). Control animals (nutritional and untreated) were reared for all treatment conditions. All pups were perfused on P10. CA1 volume, pyramidal cell density, and number were reduced in pups treated with alcohol during the third trimester-equivalent, whether unique or as exposure during all three trimesters-equivalent. CA3 volume was reduced in alcohol-treated animals across all gestational ages; however, pyramidal cell density and number in this region were only reduced in animals treated with alcohol during the third trimester-equivalent. Volume of the dentate gyrus did not appear to be affected by alcohol treatment. Granule cell density and number in this region were reduced in animals treated with alcohol during the third trimester-equivalent. The third trimester-equivalent in the rat appears to be a developmental period during which the hippocampus is particularly susceptible to the effects of alcohol consumption. The resulting damage to the hippocampus may contribute to the behavioural deficits related to learning and memory noted in children with FAS.

Adverse effects of maternal ethanol consumption on development of dorsal hippocampus in rat offspring.

We examined the laminar structure and distribution of mossy fiber terminal fields in the dorsal hippocampus, an important area for spatial learning, in rats exposed to ethanol during gestational days 10-21. Pyramidal cells in the CA3a subfield were loosely packed compared to control rats. Aberrant infra- and intrapyramidal mossy fibers were found in the CA3 region, especially in the CA3a subfield, throughout the dorsal hippocampus of ethanol-exposed rats. Aberrant mossy fiber terminals were observed more frequently in the rostral than the caudal level of the dorsal hippocampus. At the most caudal level of the dorsal hippocampus, disarrangement of pyramidal cells was seen in the CA3c subfield along with disturbed mossy fiber terminals. Immunohistochemical studies revealed that neural cell adhesion molecule (NCAM) was not related to aberrant distribution of mossy fiber terminals after prenatal exposure to ethanol. Parvalbumin immunoreactivity was increased in the dorsal hippocampus of ethanol-exposed rats compared with control rats. Abnormal development of the dorsal hippocampus induced by prenatal ethanol exposure may be associated with the defect of spatial memory seen in fetal alcohol syndrome children and their animal models.

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.

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.

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.

Independent associations among maternal alcohol consumption and infant thyroxine levels and pregnancy outcome.

Studies with animal models of alcohol-related birth defects (ARBDs) suggest that reductions in circulating thyroid hormones, including thyroxine (T4), may be a persistent postnatal effect of fetal alcohol exposure. The few clinical reports of children with fetal alcohol syndrome (FAS) that address thyroid system function generally reported that FAS children have thyroid hormone levels within normal limits. For the current study, data bases from the Fetal Alcohol Research Center and the Michigan Department of Public Health Newborn Screening Program were assessed to correlate measures of maternal drug use during pregnancy and infant outcome (gestational age at birth, birthweight, "fetal growth"), with infant whole-blood T4 levels. Multiple regression analyses accounted for demographic factors, infant age at testing, and variation in the T4 assay. As expected, alcohol intake and smoking each had a substantial negative impact on birthweight, gestational age at birth, and fetal growth, assessed as birthweight corrected for gestational age. Infant T4 levels were positively related to birthweight and gestational age and were more strongly related to fetal growth. Infant T4 levels were not influenced significantly by either maternal smoking or alcohol consumption. Smoking- and alcohol-related reductions in birthweight, gestational age, or fetal growth were not associated significantly with variations in infant T4. Interesting questions remain regarding species differences and the influences of maternal alcohol consumption on T4 metabolism as a mechanism for ARBDs. However, the current data do not support the hypothesis that maternal alcohol consumption, or smoking, during pregnancy leads to compromised thyroid system function in newborn humans.(ABSTRACT TRUNCATED AT 250 WORDS)

Maternal age and congenital optic nerve hypoplasia: a possible clue to etiology.

The maternal age of two groups of children with congenital handicaps, cerebral palsy and fetal alcohol syndrome (FAS), were examined and compared with a group of mothers of children with congenital optic-nerve hypoplasia (CONH). The maternal age of children with CONH was significantly less than for the cerebral-palsied children which, in turn, was significantly less than for the FAS children. In addition, about one-half of the children with CONH had associated handicaps which clustered into four progressively more severe combinations. Maternal age and the occurrence of endocrine problems did not differ significantly among the clusters.

Behavioral changes in rat following perinatal exposure to ethanol

Behavioral changes following pre- and postnatal ethanol administration were examined in rat pups of various ages. A significant increase in locomotor activity occurred at all ages (16, 22 and 30 days) examined. Nose poking activity in 22-day-old pups and standing activity in 30-day-old pups were also significantly higher following perinatal ethanol exposure. No significant change in grooming behavior was observed. The overactivity in rat pups following perinatal ethanol exposure is consistent with the frequently observed hyperactivity in fetal alcohol syndrome children.

Fetal Alcohol Syndrome: Implications and Counseling Considerations

This article presents the special considerations in counseling fetal alcohol syndrome children and their mothers.

Alcohol Related Birth Defects: Implications for Education

This article emerges from a larger study of preventive approaches for Alcohol Related Birth Defects (ARBD) prepared for the New York State Department of Education. The author contends that in addition to clearly identifiable Fetal Alcohol Syndrome children, there is a continuum of impairment to the offspring of drinking mothers that is dose related and produces serious behavioral/learning deficits. The continuum includes young people of normal intelligence who perform below expected levels and find school adjustment difficult. School and community agencies need to conduct studies to determine the nature and extent of impairment and the kind of interventive and preventive action that should be instituted. To that end, this article gives information on the background and nature of ARBD and some suggestions to guide development of programs.