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Findings pinpoint mechanism behind social deficits in autism
Dec 5, 2005, 04:20, Reviewed by: Dr.
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"Our findings suggest that a dysfunctional mirror neuron system may underlie the social deficits observed in autism. Together with other recent data, our results provide strong support for a mirror neuron theory of autism. This is exciting because we finally have an account that can explain all core symptoms of this disorder."
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By University of California - Los Angeles ,
New imaging research at UCLA detailed Dec. 4 as an advance online publication of the journal Nature Neuroscience shows children with autism have virtually no activity in a key part of the brain's mirror neuron system while imitating and observing emotions.
Mirror neurons fire when a person performs a goal-directed action and while he or she observes the same action performed by others. Neuroscientists believe this observation-execution matching system provides a neural mechanism by which others' actions, intentions and emotions can be understood automatically.
Symptoms of autism include difficulties with social interaction -- including verbal and nonverbal communication -- imitation and empathy. The new findings dramatically bolster a growing body of evidence pointing to a breakdown of the brain's mirror neuron system as the mechanism behind these autism symptoms.
"Our findings suggest that a dysfunctional mirror neuron system may underlie the social deficits observed in autism," said Mirella Dapretto, lead author and assistant professor in residence of psychiatry and biobehavioral sciences at the Semel Institute for Neuroscience and Human Behavior at UCLA and the David Geffen School of Medicine at UCLA. "Together with other recent data, our results provide strong support for a mirror neuron theory of autism. This is exciting because we finally have an account that can explain all core symptoms of this disorder."
Conducted at the Semel Institute's Ahmanson-Lovelace Brain Mapping Center, the research used functional magnetic resonance imaging (fMRI) to measure brain activity in 10 high-functioning children with autism while they imitated and observed 80 photos depicting different emotions such as anger, fear, happiness or sadness. In addition, the brain activity of 10 typically developing children was studied while performing the same tasks.
Separately, symptom severity of each child with autism was tested using two independent measures (the Autism Diagnostic Observation Schedule -- Generic, and the Autism Diagnostic Interview).
The study shows that unlike typically developing children, children with autism have virtually no activity in the pars opercularis of the inferior frontal gyrus, identified by previous research as a key part of the mirror neuron system. Importantly, the level of mirror neuron activity seen in children with autism was inversely related to symptom severity in the social domain.
Children with autism also showed reduced activity in the emotion centers of the brain, consistent with the hypothesis that this mirroring mechanism may play a crucial role for understanding how others feel and for empathizing with them.
All of the children rehearsed the tasks prior to the fMRI scans to assure researchers they could perform the tasks. Both groups performed equally well. Normal brain activity in areas of the brain involving sight and facial movements indicated that the children with autism remained on task during the fMRI scans. 
- Nature Neuroscience
Semel Institute for Neuroscience and Human Behavior
The research was funded primarily by a grant from the National Institute of Child Health and Human Development as part of the Collaborative Programs for Excellence in Autism.
In addition to Dapretto, the UCLA research team included Marco Iacoboni, Susan Bookheimer, Marian Sigman, Mari Davies, Jennifer Pfeifer and Ashley A. Scott. The team represents the Ahmanson-Lovelace Brain Mapping Center at the Semel Institute, the department of psychiatry and biobehavioral sciences at the Geffen School of Medicine, and the department of psychology at the UCLA College of Letters and Science.
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