Characterization of BOLD response patterns during inhibitory control in individuals with prenatal alcohol exposure

Prenatal alcohol exposure is associated with a variety of behavioral dysfunctions, including inattentiveness and impulsivity. Maladaptive behaviors such as these are associated with negative consequences including delinquency, substance abuse, and poor social adjustment. Not surprisingly, disruptive behavioral disorders are among the most frequent psychiatric diagnoses in cases of fetal alcohol exposure. In addition to other neuropsychological deficits, executive functioning impairments have been described in this population. Response inhibition is thought to be an important component of the cognitive control systems that support effective executive function. Accordingly, response inhibition impairments have been proposed as a potential mechanism underlying the inattentive and impulsive behaviors that characterize disorders such as attention- deficit/hyperactivity disorder. Although response inhibition has not been as well studied as other neuropsychological functions in individuals with fetal alcohol spectrum disorders (FASD), there is evidence from both human and preclinical studies linking gestational alcohol exposure with response inhibition deficits. This study: i) provides an account of the functional brain abnormalities underlying the disinhibited behavioral profile commonly observed in individuals with histories of prenatal alcohol exposure, and ii) investigates whether the frontal-striatal regions thought to subserve inhibitory control are disrupted by alcohol teratogenesis. Children and adolescents (ages 8-18) with (n=13) and without (n=9) histories of heavy prenatal alcohol exposure underwent functional magnetic resonance imaging while performing a response inhibition (go no-go) task. Despite similar task performance (mean response latency, accuracy, and signal detection), blood oxygenation level dependent (BOLD) response patterns differed by group. Region-of- interest analyses revealed that during task conditions that required response inhibition, alcohol-exposed participants showed greater BOLD response across several prefrontal gyri, while they showed less right caudate nucleus activation, compared to control participants. These data provide an account of response inhibition- related brain functioning in youth with FASD. Furthermore, results converge with extant literature to suggest that frontal-striatal regions important for effective inhibitory control are altered by alcohol teratogenesis