In a study that broadens our understanding of the neural basis of social interactions, researchers at Harvard Medical School and the University of Montreal have shown that individuals with autism display abnormal patterns of activity in brain circuits that underlie the understanding of other people's behavior. Autism is a neurodevelopmental disorder characterized in part by marked social deficits.
The basis of the study is a population of brain cells called mirror neurons, which are active both when we execute a specific action and when we see that action performed by another. It has been argued that mirror neurons are an essential part of recognizing actions performed by other individuals. As such, complex behaviors such as imitation, emotional processing, and language may depend on a simulation-like process whereby the observation of motor, sensory, or affective (e.g., emotional) states in others activates corresponding representations in the observer.
In the new work, researchers Hugo Théoret of the University of Montreal and Harvard Medical School and Alvaro Pascual-Leone of Harvard Medical School show that in some particular instances, brain areas that are normally active during the observation of hand movements are silent in individuals with autism. Using a technique called transcranial magnetic stimulation, the researchers showed that when autistic subjects passively viewed meaningless finger movements, brain activity in the motor cortex was unchanged from baseline values, whereas this activity was markedly enhanced in non-autistic individuals. The work suggests that a faulty mirror-neuron system could represent the neural underpinnings of the social deficits characteristic of autism, alterations that ultimately lead to reduced reciprocal social abilities and perhaps prevent the normal development of empathy.
H. Théoret, E. Halligan, M. Kobayashi, F. Fregni, H. Tager-Flusberg, and A. Pascual-Leone: "Impaired motor facilitation during action observation in individuals with autism spectrum disorder"
The members of the research team include H. Théoret of Beth Israel Deaconess Medical Center and Harvard Medical School and Hôpital Sainte-Justine and Université de Montréal; E. Halligan, M. Kobayashi, F. Fregni, and A. Pascual-Leone of Beth Israel Deaconess Medical Center and Harvard Medical School; and H. Tager-Flusberg of Boston University School of Medicine.
Publishing in Current Biology, Volume 15, Number 3, February 8, 2005, pages R84-R85. http://www.current-biology.com
The above post is reprinted from materials provided by Cell Press. Note: Materials may be edited for content and length.
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