کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2564731 | 1561034 | 2015 | 9 صفحه PDF | دانلود رایگان |
• We modeled decision-making in socio-emotional and nonsocial contexts in autism.
• Autism group lacked activation in the ventral striatum and accumbens for happy faces.
• Autism group showed hypoactivation in the frontal cortex for nonsocial response inhibition.
• Autism group showed hyperactivation in the fusiform gyrus for social response inhibition.
• Findings indicate aberrant neural processing in autism during social decision-making.
Autism is marked by impairments in social reciprocity and communication, along with restricted, repetitive and stereotyped behaviors. Prior studies have separately investigated social processing and executive function in autism, but little is known about the brain mechanisms of cognitive control for both emotional and nonemotional stimuli. We used functional magnetic resonance imaging to identify differences in neurocircuitry between individuals with high functioning autism (HFA) and neurotypical controls during two versions of a go/no-go task: emotional (fear and happy faces) and nonemotional (English letters). During the letter task, HFA participants showed hypoactivation in the ventral prefrontal cortex. During the emotion task, happy faces elicited activation in the ventral striatum, nucleus accumbens and anterior amygdala in neurotypical, but not HFA, participants. Response inhibition for fear faces compared with happy faces recruited occipitotemporal regions in HFA, but not neurotypical, participants. In a direct contrast of emotional no-go and letter no-go blocks, HFA participants showed hyperactivation in extrastriate cortex and fusiform gyrus. Accuracy for emotional no-go trials was negatively correlated with activation in fusiform gyrus in the HFA group. These results indicate that autism is associated with abnormal processing in socioemotional brain networks, and support the theory that autism is marked by a social motivational deficit.
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Journal: Progress in Neuro-Psychopharmacology and Biological Psychiatry - Volume 60, 3 July 2015, Pages 112–120