Differential Recruitment of Brain Regions During Response Inhibition in Children Prenatally Exposed to Alcohol

Abstract

Background Response inhibition is a distinct aspect of executive function that is frequently impaired in children with fetal alcohol spectrum disorders (FASD). We used a Go/NoGo (GNG) task in a functional MRI (fMRI) protocol to investigate differential activation of brain regions in the response inhibition network in children diagnosed with full or partial fetal alcohol syndrome (FAS/PFAS), compared with healthy controls. Methods A rapid, event-related task with 120 Go and 60 NoGo trials was used to study children aged 8–12 years—8 with FAS/PFAS, 17 controls. Letters were projected sequentially, with Go and NoGo trials randomly interspersed across the task. BOLD signal in the whole brain was contrasted for the correct NoGo minus correct Go trials between the FAS/PFAS and control groups. Results Compared to the FAS/PFAS group, controls showed greater activation of the inferior frontal and anterior cingulate network linked to response inhibition in typically developing children. By contrast, the FAS/PFAS group showed greater BOLD response in dorsolateral prefrontal cortex (dlPFC) and other middle prefrontal regions, suggesting compensation for inefficient function of pathways that normally mediate inhibitory processing. All group differences were significant after control for potential confounding variables. None of the effects of prenatal alcohol exposure on activation of the regions associated with response inhibition were attributable to the effects of this exposure on IQ. Conclusions This is the first FASD GNG study in which all participants in the exposed group met criteria for a diagnosis of full fetal alcohol syndrome (FAS) or partial FAS (PFAS). Although FASD is frequently co-morbid with attention deficit hyperactivity disorder (ADHD), the pattern of brain activation seen in these disorders differs, suggesting that different neural pathways mediate response inhibition in FASD and that different interventions for FASD are, therefore, warranted.

Choline and Working Memory Training Improve Cognitive Deficits Caused by Prenatal Exposure to Ethanol

“…The neural substrates recruited in children with FASD differ from those of non-exposed children in tasks that require aspects of executive function such as response inhibition [ 90 ]. Children with FASD exhibited more general activation of the frontal cortices than non-exposed children [ 90 ]. In typically developing children, the frontal cortices exhibit very selective and task specific patterns of activation [ 44 , 90 ].…”

“…Children with FASD exhibited more general activation of the frontal cortices than non-exposed children [ 90 ]. In typically developing children, the frontal cortices exhibit very selective and task specific patterns of activation [ 44 , 90 ]. Working memory and attention training in children with FASD produced positive results, improving working memory and reducing distractibility [ 12 ].…”

Fetal Alcohol Spectrum Disorders: A Review of the Neurobehavioral Deficits Associated With Prenatal Alcohol Exposure

“…Using an auditory Go/NoGo task, which assesses the number of correctly withheld responses, alcohol‐exposed children performed as well as controls in their ability to inhibit responses but had significantly slower reaction times in the Go condition (Gerhold et al., ). Neuroimaging findings also show differential patterns of regional activation in areas important for inhibition control among children with FASD (Kodali et al., ; Ware et al., ). Overall, children with FASD demonstrate deficits in response inhibition, though further research is necessary to clarify patterns of impairment.…”

Preliminary Findings that a Targeted Intervention Leads to Altered Brain Function in Children with Fetal Alcohol Spectrum Disorder

“…Research with various magnetic resonance imaging (MRI) techniques has also shown they exhibit atypical brain development [ 34 ], as evidenced by their smaller than normal global and regional brain volumes [ 35 , 36 ]; reduced size of caudate, hippocampus, and corpus callosum [ 21 , 37 , 38 ]; and abnormalities in cortical thickness and surface area [ 39 , 40 , 41 , 42 ], gyrification [ 43 , 44 ] and white matter (WM) tract formation [ 45 , 46 , 47 ]. Furthermore, studies using functional magnetic resonance imaging (fMRI) describe abnormal neural activation patterns on paradigms assessing working memory, visual search, number processing, and attention skills [ 48 , 49 , 50 , 51 , 52 , 53 ], as well as inhibitory control [ 54 , 55 , 56 , 57 ].…”