Description
The consequences of heavy prenatal alcohol exposure occur on a continuum, affecting cognitive, behavioral, and physical outcomes. Fetal alcohol syndrome (FAS) is the most severe consequence of prenatal exposure to alcohol and is diagnosed in the presence of craniofacial anomalies, growth deficiency, and central nervous system dysfunction. However, the majority of alcohol-exposed children do not meet diagnostic criteria for FAS; fetal alcohol spectrum disorders (FASD) encompass individuals affected by alcohol, including those with and without FAS. Among the cognitive deficits following prenatal alcohol exposure is perseveration, suggesting underlying response inhibition (RI) impairment. RI deficits are also supported by deficits in behavior, including high rates of disruptive disorders, including attention-deficit/hyperactivity disorder (ADHD) and conduct disorder, in addition to anatomical and functional brain abnormalities. Anatomically, research suggests that RI is associated with the middle and inferior frontal and subcortical regions. Prenatal alcohol exposure results in disproportionately reduced volumes in cortical and subcortical regions, including the prefrontal cortex and basal ganglia. Functional abnormalities are also reported in middle frontal gyrus and striatum following prenatal alcohol exposure. Although previous functional magnetic resonance imaging (fMRI) and electrophysiological studies have indicated aberrant brain functioning during a well-known response inhibition task, the go/no-go, recent studies suggest this task may measure action selection rather than RI. Thus, a more in depth investigation of neural functioning during RI is necessary to understand brain functioning and RI following prenatal alcohol exposure. The stop-signal task (SST) is hypothesized to provide a more accurate assessment of RI. The current study examined RI using the SST in alcohol-exposed and control adolescents. We hypothesized that the alcohol-exposed group would exhibit greater BOLD activation in prefrontal and subcortical areas during RI compared to controls. Subjects were two groups (ages 13-16y) of adolescents with histories of heavy prenatal alcohol exposure (AE, n=20) and unexposed controls (CON, n=20) who underwent fMRI while performing the SST. Task performance was measured using percent correct inhibits during easy, medium, and hard inhibit trials. Group differences on BOLD response were examined on 5 conditions: Allstop (all stop trials vs. Nostop trials), Easy, Medium, Hard, and Hard minus Easy. Groups were similar on demographic and behavioral outcomes, except FSIQ (AE