Summary: Reduced connectivity between the amygdala and ventrolateral prefrontal cortex has been identified in children on the autism spectrum who exhibit disruptive behaviors, compared to those on the spectrum who do not. Findings suggest this distinct brain network could be independent of core autism symptoms.
More than a quarter of children with autism spectrum disorder are also diagnosed with disruptive behavior disorders. For the first time, Yale researchers have identified a possible biological cause: a key mechanism that regulates emotion functions differently in the brains of the children who exhibit disruptive behavior.
The study appears in Biological Psychiatry: Cognitive Neuroscience and Neuroimaging.
“Disruptive behaviors such as aggression, irritability, and noncompliance are common in children with autism, and are among the main reasons for psychiatric treatment and even hospitalization,” said Denis Sukhodolsky, senior author and associate professor in the Yale Child Study Center. “Yet, little is known about the biological underpinnings of behavioral problems in children with autism.”
The first of its kind, the Yale study used fMRI scans conducted during an emotion perception task to compare the brain activity of autistic children who do and do not exhibit disruptive behavior. While in the scanner, the children were asked to view pictures of human faces that displayed calm or fearful expressions.
During the task, the researchers found reduced connectivity between the amygdala and ventrolateral prefrontal cortex — a pathway critical to the regulation of emotion — in the brains of children who exhibit disruptive behavior as compared to the brains of children who do not. “Reduced amygdala-ventrolateral prefrontal cortex functional connectivity was uniquely associated with disruptive behavior but not with severity of social deficits or anxiety, suggesting a distinct brain network that could be separate from core autism symptoms,” explained Karim Ibrahim, first author and postdoctoral fellow in the Sukhodolsky lab.
“This finding points to a brain mechanism of emotion dysregulation in children with autism and offers a potential biomarker for developing targeted treatments for irritability and aggression in autism,” said Sukhodolsky.
Other authors on this study include Jeffrey A. Eilbott, Pamela Ventola, George He, Kevin A. Pelphrey, and Gregory McCarthy.
About this neuroscience research article
Source: Yale Media Contacts: Kendall Teare – Yale Image Source: The image is in the public domain.
Reduced Amygdala–Prefrontal Functional Connectivity in Children With Autism Spectrum Disorder and Co-occurring Disruptive Behavior
Background Disruptive behaviors are prevalent in children with autism spectrum disorder (ASD) and often cause substantial impairments. However, the underlying neural mechanisms of disruptive behaviors remain poorly understood in ASD. In children without ASD, disruptive behavior is associated with amygdala hyperactivity and reduced connectivity with the ventrolateral prefrontal cortex (vlPFC). This study examined amygdala reactivity and connectivity in children with ASD with and without co-occurring disruptive behavior disorders. We also investigated differential contributions of externalizing behaviors and callous-unemotional traits to variance in amygdala connectivity and reactivity.
Methods This cross-sectional study involved behavioral assessments and neuroimaging in three groups of children 8 to 16 years of age: 18 children had ASD and disruptive behavior, 20 children had ASD without disruptive behavior, and 19 children were typically developing control participants matched for age, gender, and IQ. During functional magnetic resonance imaging, participants completed an emotion perception task of fearful versus calm faces. Task-specific changes in amygdala reactivity and connectivity were examined using whole-brain, psychophysiological interaction, and multiple regression analyses.
Results Children with ASD and disruptive behavior showed reduced amygdala–vlPFC connectivity compared with children with ASD without disruptive behavior. Externalizing behaviors and callous-unemotional traits were associated with amygdala reactivity to fearful faces in children with ASD after controlling for suppressor effects.
Conclusions Reduced amygdala–vlPFC connectivity during fear processing may differentiate children with ASD and disruptive behavior from children with ASD without disruptive behavior. The presence of callous-unemotional traits may have implications for identifying differential patterns of amygdala activity associated with increased risk of aggression in ASD. These findings suggest a neural mechanism of emotion dysregulation associated with disruptive behavior in children with ASD.