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Imitation, mirror neurons and autism
J H Williams1, A Whiten, T Suddendorf
1Department of Child Health, University of Aberdeen, Foresterhill, Aberdeen AB25 2ZD, UK. justin.williams@abdn.ac.uk
Neuroscience and Biobehavioral Reviews
|July 11, 2001
Summary
Difficulties in imitation and mimicking, such as echolalia, may explain autism. Failures in mirror neuron (MN) systems, which bridge self and other actions, could lead to developmental impairments seen in autism.
Area of Science:
- Neuroscience
- Developmental Psychology
- Cognitive Science
Background:
- Autism spectrum disorder (ASD) is characterized by cognitive deficits, but these offer incomplete explanations.
- Imitative disturbances, including difficulties in action copying and stereotyped mimicking (e.g., echolalia), are prominent in ASD.
- Mirror neurons (MNs), found in frontal cortex, activate for both self-performed and observed actions, potentially bridging self-other representations.
Purpose of the Study:
- To investigate the role of mirror neuron (MN) systems in the imitative disturbances associated with autism.
- To propose a neurodevelopmental model for autism centered on MN system dysfunction.
Main Methods:
- The study proposes a theoretical framework linking MN function to imitation and social cognition.
- It reviews existing literature on MNs, imitation, and autism.
Main Results:
- Mirror neuron systems provide a potential neural basis for understanding imitative deficits in autism.
- The evolution of sophisticated cortical systems utilizing MNs is crucial for social cognitive functions.
- Early developmental failures in MN systems may trigger a cascade of impairments leading to the autism syndrome.
Conclusions:
- Dysfunction within mirror neuron systems is hypothesized as a key factor in the development of autism.
- This perspective offers a novel explanation for the imitative and social challenges observed in individuals with autism.
- Understanding MN system development is critical for addressing the neurodevelopmental underpinnings of autism.