Prenatal exposure to alcohol may cause temporal processing deficits

December 16, 2002

Fetal Alcohol Syndrome (FAS) is diagnosed on the basis of three criteria: growth retardation, characteristic craniofacial anomalies, and central nervous system (CNS) dysfunction. Most alcohol-exposed children do not qualify for a 'full' FAS diagnosis, yet demonstrate a wide range of neurobehavioral effects that presumably reflect underlying CNS structural and functional changes. While numerous studies have shown that the basal ganglia and cerebellum regions are affected by alcohol exposure, few studies have examined whether there is neurobehavioral evidence of those effects. A study in the December issue of Alcoholism: Clinical & Experimental Research examines performance on two types of timing tasks in order to determine the extent to which prenatal alcohol exposure affects perception, movement planning, and movement execution during tasks that require temporal processing.

"Both the basal ganglia and cerebellum regions of the brain play a role in motor planning and execution," said Tara S. Wass, assistant professor of child and family studies at The University of Tennessee and corresponding author for the study. "In addition, they both influence cognitive functioning." Abnormalities in these brain structures, she said, have been observed in several conditions. For example, basal ganglia abnormalities have been noted in individuals with Parkinson's or Huntington's Disease, as well as attention deficit hyperactivity disorder (ADHD). Abnormalities in the cerebellum have been documented in children with ADHD or autism.

"Studies from adult patients with damage to the basal ganglia or the cerebellum indicate that temporal processing is impaired in these populations," said Wass. "Temporal information is inherent to the events we experience and the activities we engage in, such as catching a ball, accurate perception of speech or music, planning an activity, or anticipating when things are likely to occur. We know very little about temporal processing in alcohol-affected individuals, although some deficits we observe in them - in the areas of balance, and fine and gross motor skills - could be caused in part by deficits in temporal planning. So far, very few studies have examined whether alcohol-affected children exhibit deficits that would be predicted by changes in these structures." Wass added that one of the few studies in this area found that alcohol-affected children exhibited poorer balance than non-exposed children.

Researchers examined two groups of children ages five to 10 years: 14 with confirmed heavy prenatal alcohol exposure (1 met the diagnostic criteria for FAS, 13 did not) and 22 controls (without prenatal exposure). The children completed two timing tasks: a coincident-anticipation timing task that primarily assessed central processing, and a movement-speed timing task that evaluated the motor component of temporal processing. Wass said that both tasks are easily understood by young children, even those who are cognitively impaired, and allowed researchers to "break performance up into component parts" in order to try to pinpoint where the underlying deficits might exist.

"We found that alcohol-exposed children were impaired in their ability to perceive and utilize temporal information to complete simple tasks," said Wass. "Alcohol-affected children tended to be much more variable and much less accurate than non-exposed children in their ability to perceive and utilize temporal information."

"These children have slower and less efficient responses in general," said Claire D. Coles, professor of psychiatry and behavioral sciences at the Emory University School of Medicine. Although alcohol-affected individuals often show relative deficits in visual/motor integration, processing speed and reaction time, she noted, "this study examines these processes separately and provides more information about how alcohol-affected individuals function in these areas."

Coles added that, even though the study did not examine the perceptual component of temporal responses, "this area is probably impaired as well," she said. "In addition, it is of significance that the children tested had lower IQs and that their performance IQ, based on reaction time and visual/motor processing, was particularly impaired. Such individuals learn more slowly, have less confidence in their own perceptions and reactions, perform less accurately, and find the world a consistently more confusing and difficult place than do their contemporaries. Deficits in these basic processes translate into functional deficits in academics, vocational, adaptive and social skills. Also of interest is the lack of an 'impulsivity' effect. My own research has regularly not found any impulsivity effect and this is a confirmation of that. It is important to do these kinds of experimental studies to examine the actual 'neurobehavior' of alcohol-affected individuals instead of relying on clinical lore that attributes ADHD-like behavior to this group, probably inaccurately."

"We are still learning about the range of problems that children with heavy prenatal alcohol exposure may experience," said Wass. "The present data indicate that temporal processing is impaired in these children. Additional research is warranted because it would be helpful if we could begin to identify a pattern of consistent neurobehavioral deficits observed in alcohol-affected children that is distinct from the pattern of deficits observed in children with other developmental disorders. A first step in doing this would be to use what we know about the neuroanatomical changes that follow alcohol exposure as a guide for identifying abilities that may be impaired."

In addition, said Coles, "we need more perceptual/motor studies that can be related to specific academic and adaptive deficits. Furthermore, understanding these functional deficits may suggest areas of functional and structural deficits in the brain than can be examined in imaging studies. However," she cautioned, "I think it is important not to over generalize from such studies. The implication of this paper - that damage to specific brain regions underlies the functional deficits observed - is still speculation at this time."
-end-
Co-authors of the Alcoholism: Clinical & Experimental Research paper included: Roger W. Simmons of the Motor Control Laboratory in the Department of Exercise and Nutritional Sciences at San Diego State University; and Jennifer D. Thomas and Edward P. Riley of the Center for Behavioral Teratology in the Department of Psychology at San Diego State University. The study was funded by the National Institute on Alcohol Abuse and Alcoholism.

Alcoholism: Clinical & Experimental Research

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