International Meeting for Autism Research (London, May 15-17, 2008): Dysfunctional mirror neurons and Autism A doubtful connection

Dysfunctional mirror neurons and Autism A doubtful connection

Thursday, May 15, 2008
Champagne Terrace/Bordeaux (Novotel London West)
10:30 AM
I. Dinstein , Neuroscience, New York University, New York, NY
C. Thomas , Martinos Center at MGH, Harvard Medical School, Charlestown, MA
K. Humphreys , Psychology, Institute of Psychiatry, London, United Kingdom
N. J. Minshew , Departments of Psychiatry and Neurology, University of Pittsburgh School of Medicine, Pittsburgh, PA
M. Behrmann , Psychology, Carnegie Mellon University, Pittsburgh, PA
D. J. Heeger , Psychology and Neuroscience, New York University, New York, NY
Background: It has been hypothesized that core symptoms in autism result from a specific dysfunction in mirror neuron activity. However, the experimental protocols commonly used to assess mirror neuron activity in humans are not capable of isolating their responses from the many other visual and motor neurons that coexist in the same cortical areas.
Objectives: To better isolate mirror neuron responses in high functioning individuals with autism we used an fMRI adaptation protocol designed to assess the selectivity of neurons for observed and executed movements; a defining feature of mirror neuron physiology.
Methods: In the first experiment, subjects were asked to observe, execute, or imitate the rock, paper, and scissors hand movements (from the children’s game). Activity during each condition was compared with rest to assess “mirror system” activity. In the other experiments, subjects were asked to observe or execute a single repeating hand posture or a sequence of different hand postures. Activity during blocks of different postures was compared with that of repeated posture to measure visual and motor adaptation.
Results: Responses across the whole cortex including candidate mirror system areas (defined using the common imitation protocol: anterior intraparietal sulcus and ventral premotor) were comparable across autism and comparison groups in all three experiments. Individuals with autism, however, exhibited more variable fMRI responses both within and across subjects, across the whole cortex.
Conclusions: High functioning individuals with autism exhibited normal cortical responses, on average, in candidate mirror system areas. Furthermore, these individuals exhibited fMRI adaptation during both observation and execution of movements, indicative of normal underlying movement-selective neural responses. Such selective responses are crucial for proper movement perception as hypothesized by “mirror system” theories. Our results therefore suggest that dysfunctional mirror neurons are not the underlying physiological basis of core autism symptoms.
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