Deficits associated with prenatal alcohol exposure can be seen as early as infancy

March 14, 2004

Most of the research on arousal and attention deficits caused by prenatal alcohol exposure has been conducted with children. An innovative new study, published in the March issue of Alcoholism: Clinical & Experimental Research, examines different components of attention through use of heart-rate data collected from six-month-old infants whose mothers drank during pregnancy. The findings indicate that slower processing speeds and arousal-regulation problems exist as early as infancy.

"The postnatal environment that children experience has a tremendous impact on children's cognitive status and attentional regulation skills," explained Julie A. Kable, assistant professor at Emory University School of Medicine and first author of the study. "Children of women who consume large amounts of alcohol during pregnancy and/or are substance abusers often experience family environments that do not support optimal development. As a result, when you examine older children it is often difficult to partition out the impact of the prenatal exposure with the impact of the postnatal environment. Assessments conducted closer in time to the insult provide a more accurate picture of the teratogenic effect."

"From a clinical point of view," added Sandra W. Jacobson, a professor in the department of psychiatry and behavioral neurosciences at Wayne State University School of Medicine, "tests such as the ones used in this study are important since it is critical to identify affected children as early in infancy as possible. Interventions are more likely to prove effective when implemented early in development and when specific core deficits are identified and can be targeted."

Research participants (n=118 infants) were recruited from the larger Atlanta-based Fetal Growth and Development Study, a project designed to estimate the prevalence of Fetal Alcohol Syndrome. Researchers used structured interviews to gather demographic, pregnancy-related, and alcohol and other drug-use information from the mothers; their infants were given an extensive physical examination; and medical records of the pregnancy and delivery were also collected. Based on the reported drinking habits of the mothers, infants were divided into two groups: high risk (n=18) and low risk (n=100). While sitting in a car seat, each infant was presented with both auditory (400 and 1,000 hertz pure tones) and visual stimuli (chromatic Caucasian faces), and his/her cardiac responses were recorded.

"One of the most important cognitive processes is learning to regulate arousal level in order to appropriately take in new information or learn from the world around you," said Kable. "This study found that prenatal alcohol exposure resulted in disruption of this fundamental cognitive process."

Specifically, infants identified as "high risk" had significantly higher levels of arousal yet responded more slowly to stimuli than did infants identified as "low risk." Higher levels of behavioral arousal, coupled with lower neurophysiological responses involved in encoding environmental stimuli and initiating attention, suggest that "high risk" infants have difficulties with regulating interactions between arousal levels and the attentional system that processes environmental events.

"[These results] provide evidence of less efficient neurophysiological encoding of information in infants in the high-risk alcohol and drug exposure group," noted Jacobson. "These infants were more likely to have specific deficits in processing speed ... [which] is consistent with our previous reports of slower processing speed in infants. These infant findings confirm the data reported for older children, namely, that sustained attention by alcohol exposure is not affected while processing speed is. [Furthermore,] the deficit in this high-risk group is associated with both visual and auditory attention, while the previous studies had only examined visual responses. More research will be needed to determine whether the auditory deficit is attributable to the alcohol or smoking exposure."

"The long-term implications of these findings are impairments in cognitive and later attentional regulation skills," added Kable. "If one does not maximize learning efficiency then he or she experiences a cumulative deficit over time. The cognitive deficits will result in lowered IQ scores and difficulties with learning basic functional and academic skills. The arousal difficulties may result in behavioral disturbances and meltdowns from being over-aroused and not being able to appropriately calm down when needed."

These findings also help illuminate a somewhat controversial area of alcohol research, the differences and similarities between children exposed to alcohol and those clinically diagnosed with Attention Deficit Hyperactivity Disorder (ADHD).

Jacobson elaborated: "[In previous research, co-author Claire D.] Coles has shown that alcohol-exposed children seem to have fewer problems with sustained attention and more with working memory than do children with ADHD. [Other research has] found that alcohol-exposed infants were chronically more aroused and stressed than non-exposed infants, findings consistent with the behavioral assessment of increased arousal reported by Drs. Kable and Coles. Although ... it is reasonable to consider that higher arousal and slower responses to stimuli may contribute to poorer long-term cognitive potential, it is premature to link these deficits to ADHD, particularly since the alcohol-related attention deficits seen in these infants and in older children do not include the sustained attention and hyperactivity problems characteristic of ADHD. New research is investigating different ADHD subgroups, those with and without hyperactivity. It may be that alcohol exposure during pregnancy contributes to the incidence of ADHD-like deficits in children with attention problems that lack hyperactivity disorder. If so, the new findings presented by Drs. Kable and Cole are very important in that they permit the identification of these children in infancy."

"I do think that the behavioral manifestations of the neurodevelopmental damage to alcohol-affected children can resemble those of children with ADHD," added Kable, "but the neurodevelopmental origins of the behavioral problems differ. It is not yet clear what this means for treatment because the efficacy of medications has not been evaluated in alcohol-affected children."
-end-
Alcoholism: Clinical & Experimental Research (ACER) is the official journal of the Research Society on Alcoholism and the International Society for Biomedical Research on Alcoholism. The co-author of the ACER paper was Claire D. Coles of the Marcus Institute, an affiliate of Kennedy Krieger Institute at Emory University, and of the Department of Pediatrics as well as the Department of Psychiatry and Behavioral Sciences, both at Emory University School of Medicine. The study was partially funded by the Center for Disease Control and Prevention.

Alcoholism: Clinical & Experimental Research

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