Description
Prenatal alcohol exposure is associated with many neurobehavioral deficits, including verbal learning and memory impairments. Previous research suggests these impairments represent deficient encoding processes but intact retrieval systems. The current study aimed to 1) evaluate these findings in comparison to an unexposed clinical contrast group, as well as a typically developing control group, and 2) extend these findings to a younger sample. Subjects were 300 children; 100 with prenatal alcohol exposure (AE), 100 non-exposed and developing typically (T-CON), and 100 non-exposed with a behavioral or developmental concern (B-CON). Fifty children in each of these subject groups were between the ages of five and seven, and the other fifty were between the ages of ten and sixteen. Performance on the California Verbal Learning Test — Children's Version (CVLT-C) was analyzed using standard analysis of variance (ANOVA) techniques and a 3 (group) x 2 (age) design. All subject groups had improved recall after repeated exposure to the verbal stimuli (Trial A5 > Trial A1). Across ages, group differences were found on the learning trials (AE < B-CON < T-CON). Within trials, group differences were observed on the first (AE < B-CON & T-CON; B-CON = T-CON), and the last trial (AE < B-CON < T-CON). Across ages, groups also differed on free recall after a delay (AE < B-CON < T-CON). However, when the amount of learned information was accounted for (retention), these group differences on the delayed recall trial disappeared. When tested by age, rates of retention were the same across groups for the younger children, despite group differences on delayed recall (AE & B-CON < T-CON), but group differences were detected in the older children even after accounting for the amount of learned information (delayed recall: AE < B-CON & T-CON; retention: AE < B-CON; T-CON = AE & B-CON). Group differences were also found for recognition discriminability across ages (AE & B-CON < T-CON). Across subject groups, older children had better learning, recall, retention, and recognition discriminability than younger children. These findings further support the notion that memory deficits observed in children with prenatal alcohol exposure may be due to encoding deficits and not to retrieval problems, but suggest that with age, non-exposed children may develop more efficient retention strategies. These findings also demonstrate that recognition discriminability might not be useful to identify children with prenatal alcohol exposure from other clinical populations when exposure history is unknown.
