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Biomedical subjects

E P Riley

Publications and source records attributed to E P Riley.

At least 37 records · Page 2Linked to original sources
PubMed1998

Neonatal alcohol exposure produces hyperactivity in high-alcohol-sensitive but not in low-alcohol-sensitive rats.

Children of women who consume high amounts of alcohol during their pregnancies vary greatly in physical and behavioral outcomes. Although many factors, such as dose and timing of exposure, undoubtedly contribute to this variation, one important determinant may be genetic differences in the response to alcohol. The present study examined activity levels in high alcohol sensitivity (HAS) and low alcohol sensitivity (LAS) rats following neonatal alcohol exposure. These lines were selectively bred for extremes in ethanol-induced "sleep times." The HAS and LAS offspring were exposed to alcohol via an artificial rearing procedure using the "pup-in-the-cup" technique. Rat pups were exposed to ethanol (6 g/kg/day) from postnatal day (PD) 4 through 7 and faded to a dose of 3 g/kg/day on PD 8 and 9. An artificially reared gastrostomy control group (GC) and a normally reared suckle control group (SC) were also included. Activity level was measured on PD 18 through PD 21 for 30 min daily in automated activity monitors. Neonatal ethanol exposure produced overactivity in HAS rats, relative to their controls, but the same ethanol treatment had no effect on the LAS rats. Importantly, there were no differences in blood alcohol concentrations (around 420 mg/dl) between the two lines during the treatment period. These data suggest that genetic differences in response to alcohol may be a predictor for some of the behavioral teratogenic effects of alcohol.

Animals↗
PubMed1998

Neuropsychological comparison of alcohol-exposed children with or without physical features of fetal alcohol syndrome.

Fetal alcohol syndrome (FAS) is associated with behavioral and cognitive deficits. However, the majority of children born to alcohol-abusing women do not meet the formal criteria for FAS and it is not known if the cognitive abilities of these children differ from those of children with FAS. Using a set of neuropsychological tests, 3 groups were compared: (a) children with FAS, (b) children without FAS who were born to alcohol-abusing women (the PEA group), and (c) normal controls. The results indicated that, relative to controls, both the FAS and the PEA groups were impaired on tests of language, verbal learning and memory, academic skills, fine-motor speed, and visual-motor integration. These data suggest that heavy prenatal alcohol exposure is related to a consistent pattern of neuropsychological deficits and the degree of these deficits may be independent of the presence of physical features associated with FAS.

Adolescent↗
PubMed1998

A review of the neurobehavioral deficits in children with fetal alcohol syndrome or prenatal exposure to alcohol.

Fetal alcohol syndrome is a devastating developmental disorder caused by prenatal exposure to high amounts of alcohol. In addition to structural abnormalities and growth deficits, fetal alcohol syndrome is associated with a broad spectrum of neurobehavioral anomalies. This paper reviews the behavioral and cognitive effects of prenatal alcohol exposure. More than 20 years of research are discussed, with a focus on IQ, activity, attention, learning, memory, language, motor, and visuospatial abilities in children prenatally exposed to varying amounts of alcohol, including those with fetal alcohol syndrome.

Alcohol Drinking↗
PubMed1998

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 callosum, 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.

Alcohol Drinking↗
PubMed1998

Fetal alcohol syndrome: does alcohol withdrawal play a role?

Alcohol use by a pregnant woman may interfere with the development of her fetus. Newborns whose mothers are intoxicated during delivery can experience withdrawal symptoms, such as tremors and even seizures. It is likely that withdrawal also can occur during fetal development. Thus, the possibility exists that withdrawal by the pregnant woman may exacerbate alcohol's adverse effects on her fetus. One potential mechanism through which alcohol withdrawal might damage the fetus involves the receptor for the neurotransmitter glutamate (i.e., the N-methyl-D-aspartate [NMDA] receptor). This receptor plays a crucial role during neuronal development. Excessive activation of the NMDA receptor, which occurs during withdrawal, may lead to neuronal cell death. Animal studies suggest that these effects may contribute to behavioral deficits following prenatal exposure to alcohol.

Animals↗
PubMed1998

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.

Adolescent↗
PubMed1998

Comparison of social abilities of children with fetal alcohol syndrome to those of children with similar IQ scores and normal controls.

Children diagnosed with fetal alcohol syndrome (FAS) were assessed with items from the social skills domain of the Vineland Adaptive Behavior Scales (VABS) via interviews with their caregivers. Their scores were compared with scores from children in two control groups. The control groups included children matched for IQ to the FAS group (specifically on verbal IQ, henceforth, the VIQ group) and children with IQ scores in the average to above-average range (normal control group). Forty-five children (age range, 5 years 7 months to 12 years 11 months) were assessed (n/group = 15). All groups differed with regard to social ability, as measured by the VABS (NC > VIQ > FAS), even when the effects of socioeconomic status were held constant. The three subdomains of the VABS social scale (interpersonal relationship skills, use of play and leisure time, and coping skills) were assessed, and results showed that the children with FAS were most impaired on the subdomain that assessed interpersonal relationship skills. An additional measure was constructed by obtaining an age-equivalent score for the VABS social scale and calculating a difference score by subtracting the child's chronological age from his/her age-equivalent score. There was a significant correlation between chronological age and difference scores for children in the FAS group but not for children in the two control groups. Specifically, in older children with FAS, there was an increased discrepancy between their ages and their age-equivalent scores, a discrepancy that was not present in children in the control groups. These results suggest that social deficits in children with FAS are beyond what can be explained by low IQ scores and indicate that there may be arrested, and not simply delayed, development of social abilities in children with FAS.

Child↗
PubMed1998

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.

Adolescent↗
PubMed1997

Heavy prenatal alcohol exposure with or without physical features of fetal alcohol syndrome leads to IQ deficits.

OBJECTIVE: To assess general intellectual functioning in children with histories of heavy prenatal alcohol exposure, with or without the facial features and growth deficiencies characteristic of fetal alcohol syndrome (FAS). DESIGN: Forty-seven alcohol-exposed children were recruited on evaluation at a dysmorphology clinic and evaluated as part of a university research project using standard tests of IQ. Thirty-four of the alcohol-exposed patients met the traditional diagnostic criteria for FAS. The other 13 alcohol-exposed children lacked both the pattern of facial features and prenatal or postnatal growth deficiency characteristic of the diagnosis. RESULTS: Compared with normal control subjects matched for age, sex, and ethnicity, both groups of alcohol-exposed children displayed significant deficits in overall IQ measures and deficits on most of the subtest scores. Although those in the nondysmorphic group usually obtained marginally higher IQ scores than those in the FAS group, few significant differences were found between the two alcohol-exposed groups. CONCLUSIONS: These results indicate that high levels of prenatal alcohol exposure are related to an increased risk for deficits in intellectual functioning and that these can occur in children without all of the physical features required for a diagnosis of FAS. They also emphasize the need for conducting a thorough history of prenatal alcohol exposure in children with intellectual deficits.

Child↗
PubMed1997

Effects of neonatal exposure to nicotine on electrophysiological parameters in adult rats.

In clinical studies and animal models, there is evidence that nicotine exposure during gestation can result in deficits in cognitive performance. The present study examined the effects of two doses of neonatal nicotine exposure on adult brain activity as assessed by the N1 and P3 components of the event-related potential (ERP) and background electroencephalography (EEG). Nicotine (0 mg, 1 mg/kg/day, 4 mg/kg/day) was administered to neonatal rat pups from postnatal day 4 (PN4) through PN12 with an artificial rearing paradigm; suckled rats served as additional control subjects. Nicotine exposure was specifically found to alter responses of the P3 component of the ERP, recorded in dorsal hippocampus, to changes in stimulus parameters. A significant reduction in the response of the P3A component to the noise tone as compared with the level of the frequently presented tone was found. A significant reduction in the response to the noise tone as compared with the level of the infrequently presented tone also was seen in the P3B component. No effects of drug exposure were found on the N1 component in any lead, although artificial rearing produced specific effects on the latency of the N1 component in cortex. No significant differences among treatment groups were found on any of the EEG-dependent variables. Female rats overall were found to have significantly higher EEG amplitudes than the males, a finding previously reported in our laboratory. However, no overall effects of gender were found on any ERP component. These studies suggest that neonatal nicotine exposure specifically reduces the electrophysiological response of the hippocampus to changes in auditory stimuli. Additional studies will be necessary to link these P3 amplitude changes to the effects of nicotine on the developing brain in human and animal subjects.

Acoustic Stimulation↗
PubMed1997

MK-801 administration during ethanol withdrawal in neonatal rat pups attenuates ethanol-induced behavioral deficits.

Alcohol exposure during development can produce central nervous system dysfunction, resulting in a wide range of behavioral alterations. The various mechanisms by which alcohol causes these behavioral changes, however, remain unknown. One mechanism that has been suggested is NMDA receptor-mediated excitotoxic cell death produced by ethanol withdrawal. The present study examined whether MK-801, an antagonist of the NMDA receptor that has been shown to protect against NMDA receptor-mediated excitotoxicity, could block alcohol's adverse effects on behavior. Sprague-Dawley rat pups were exposed to alcohol (6.0 g/kg) in a binge-like manner on postnatal day 6 using an artificial rearing procedure. Subjects then received an injection of MK-801 (0.1 mg/kg) or vehicle during withdrawal, 21 hr after ethanol exposure. At postnatal day 40, all subjects were tested on a serial spatial discrimination reversal task. Ethanol-exposed subjects were impaired in both discrimination and reversal learning, and committed a significantly greater number of perseverative-type errors, compared with controls. MK-801 administration during ethanol withdrawal significantly attenuated ethanol-induced deficits in reversal learning and increases in perseverative-type errors, whereas MK-801 exposure by itself had no significant effect on performance. Thus, exposure to MK-801 during ethanol withdrawal partially protected against alcohol-related disruptions in spatial reversal learning. These results support the suggestion that NMDA receptor-mediated excitotoxicity may be one mechanism by which alcohol induces behavioral teratogenicity.

Alcohol Withdrawal Delirium↗
PubMed1996

EEG findings in fetal alcohol syndrome and Down syndrome children.

Results from previous studies evaluating the electroencephalograms (EEGs) of infants born to alcoholic mothers suggest that the neonatal EEG may be a sensitive measure of prenatal ethanol exposure. Few studies, however, have examined EEG records of adolescent children with fetal alcohol syndrome (FAS). The present study investigated the resting EEG recordings of 18 matched triads of FAS, Down syndrome, and normal control subjects. Significant reductions in mean power of the alpha frequencies (7.5-12 Hz) were seen for both clinical groups, however, each syndrome appeared to have distinct EEG spectral distributions. Down syndrome children overall had diffuse EEG slowing while the EEG records of the FAS children showed reduced power, particularly in the alpha frequencies in the absence of significant slow activity. In the Down syndrome children, significant decreases in alpha power was seen in posterior cortical regions, whereas FAS children were more affected in the left hemisphere. This study suggests that certain EEG variables may be helpful in characterizing the neurophysiology of FAS.

Adolescent↗
PubMed1996

Abnormal development of the cerebellar vermis in children prenatally exposed to alcohol: size reduction in lobules I-V.

Abnormalities of the cerebellar vermis have been well documented in animal models of fetal alcohol syndrome. At this point, it is not known if the same brain region is affected in humans prenatally exposed to alcohol. In this study, the area of the cerebellar vermis was measured from brain magnetic resonance images of 9 children and young adults with prenatal alcohol exposure and 24 control subjects in the same age range. Six of the exposed children met standard criteria for fetal alcohol syndrome. The remaining three subjects had significant histories of prenatal exposure to alcohol, but did not have enough of the classic facial features for the diagnosis. For each subject with a suitable midsagittal section, three vermal areas were circumscribed: anterior vermis (vermal lobules I-V), posterior vermis (vermal lobules VI and VII), and the remaining vermal area (including lobules VIII-X). Statistical analyses revealed that the anterior region of the vermis was significantly smaller in subjects with prenatal alcohol exposure, whereas the posterior region and the remaining vermal area did not differ between groups. Previous findings from an animal model of neonatal alcohol exposure have documented Purkinje cell loss in vermal lobules I-V and IX-X, with notable sparing in lobules VI-VII. Thus, the results of both studies indicate similar patterns of abnormal brain development in the anterior vermal region, with apparent sparing in the posterior vermal region. Our findings, for the first time, suggest that regionally specific Purkinje cell death may also occur in humans prenatally exposed to alcohol.

Adolescent↗
PubMed1996

Auditory event-related potentials in fetal alcohol syndrome and Down's syndrome children.

Abnormal or borderline electroencephalograms are commonly observed in cases of gross mental retardation. However, fewer studies have focused on the use of event-related responses to aid in the differential diagnosis of developmental cognitive disorders. Fetal alcohol syndrome (FAS) and Down syndrome represent the most common known causes of mental retardation in the Western world. Although Down syndrome is easily diagnosed with a chromosome assay, FAS can be more difficult to diagnose since the diagnostic features are more subjectively based. The present study is the first to characterize auditory event-related potentials (ERPs) in children with FAS and contrast them to subjects with Down syndrome and controls. A passive auditory "oddball-plus-noise" paradigm was utilized to elicit ERPs. Parietal P300 latencies in response to the noise-burst stimuli for the FAS children were significantly longer, as were the P300s from all cortical sites in Down syndrome subjects in response to the both the infrequent tone and noise-burst stimuli when compared with the controls. Frontal P300s in Down syndrome children were significantly larger in amplitude compared to the controls and FAS children in response to the infrequent tone. A discriminant function analysis also revealed that these children could be correctly classified as being either Down syndrome, FAS, or normal controls using measures of latency and amplitude of the P300. These data suggest that an evaluation of ERP characteristics may provide a better understanding of the differences between FAS and Down syndrome children, and prove to be an aid in the early identification of children with FAS. These results demonstrate neurophysiological differences between FAS and Down syndrome, and suggest that P300 amplitude and latency data collected from a passive ERP task may be helpful in the discrimination of developmental cognitive disorders.

Adolescent↗
PubMed1996

A decrease in the size of the basal ganglia in children with fetal alcohol syndrome.

Magnetic resonance imaging was conducted on six children and adolescents with fetal alcohol syndrome and seven matched normal controls. Detailed volumetric analyses demonstrated significant reductions in the cerebral vault, basal ganglia, and diencephalon in the children with fetal alcohol syndrome, compared with control children. In addition, the volume of the cerebellar vault was smaller than controls in 4 of the 6 children with fetal alcohol syndrome, although the group difference did not reach significance. When the basal ganglia were divided into the caudate and lenticular nuclei, both of these regions were significantly reduced in the children with fetal alcohol syndrome. Finally, when the overall reduction in brain size was controlled, the proportional volume of the basal ganglia and, more specifically, the caudate nucleus was reduced in the children with fetal alcohol syndrome. These results may relate to behavioral findings in both humans and animals exposed to alcohol prenatally.

Adolescent↗
PubMed1996

Verbal learning and memory in children with fetal alcohol syndrome.

Children with fetal alcohol syndrome (FAS) were administered the California Verbal Learning Test-Children's Version, a word list learning task that assesses immediate and delayed recall and recognition memory. When compared with matched control children, the children with FAS had difficulty learning and recalling the words after a delay period and tended to make an increased number of intrusion and perseverative errors. In addition, they had difficulty discriminating target words from distracter words and made more false-positive errors on recognition testing. Some of these deficits persisted even when mental age was controlled. The results suggest that children with FAS have profound verbal learning and memory deficits, and that some of these deficits cannot be accounted for even when mental age is considered. Furthermore, the results are consistent with deficits in encoding verbal information and impairment in response inhibition capabilities.

Adolescent↗