Object and spatial memory in fetal alcohol syndrome: An assessment of hippocampal dysfunction.

Fetal alcohol syndrome (FAS), a leading cause of mental retardation, was initially described in the United States only twenty years ago. Because it is likely that fetal alcohol exposure contributes substantially to the heterogeneously-grouped learning disabled population, it is worthwhile to review the known cognitive and neurobiological bases of this syndrome, and to test promising neuropsychological hypotheses. For example, animal models of FAS indicate neuroanatomical and behavioral deficits attributable to dysfunction of the hippocampus, a neural structure important in learning and especially spatial memory. In addition, although humans with FAS have demonstrated difficulty with nonverbal problems that are spatial in nature, no specific tests of hippocampal dysfunction have been administered. Thus, fifteen children (x age = 9.8 ± 2.32) with alcohol related birth defects (ARBD), and 15 control children (x age = 9.7 ± 2.40) were tested on several spatial and object memory tasks. These tasks were administered in (1) a small-scale desk-work type environment, and (2) a large-scale environment designed to parallel animal work. The spatial tasks were presumed to be indicators of intact hippocampal functioning, but the object memory tasks were not. As expected, individuals with ARBD consistently demonstrated a deficit spatial memory performance. There was never a significant difference on an immediate object recall task, but the children with ARBD tended "to forget" more objects after a delay in two of the three experiments. Previous research emphasizes the role of the hippocampus in spatial memory (Morris, Garrud, Rawlins, & O'Keefe, 1982) as well as in visually-mediated delayed object recall. Left neocortical structures that subserve immediate object recall appear to be relatively intact. Visuospatial descriptive testing indicated a further disturbance in nonverbal information processing that could involve such neuroanatomical structures as the frontal lobe, parietal cortex, basal ganglia, corpus callosum, and cerebellum. Further studies that address intact vs. deficit performance in children with ARBD could illuminate some specific structural-functional attributes in the brains of children. Defining the neurodevelopmental role of the hippocampus in learning and memory is a priority to be accomplished