Mirror neuron activity associated with social impairments but not age in autism spectrum disorder.

Monash Alfred Psychiatry Research Centre, School of Psychology and Psychiatry, Monash University and the Alfred, Melbourne, Australia.
Biological psychiatry (Impact Factor: 8.93). 03/2012; 71(5):427-33. DOI: 10.1016/j.biopsych.2011.09.001
Source: PubMed

ABSTRACT The neurobiology of autism spectrum disorder (ASD) is not particularly well understood, and biomedical treatment approaches are therefore extremely limited. A prominent explanatory model suggests that social-relating symptoms may arise from dysfunction within the mirror neuron system, while a recent neuroimaging study suggests that these impairments in ASD might reduce with age.
Participants with autism spectrum disorder (i.e., DSM-IV autistic disorder or Asperger's disorder) (n = 34) and matched control subjects (n = 36) completed a transcranial magnetic stimulation study in which corticospinal excitability was assessed during the observation of hand gestures.
Regression analyses revealed that the ASD group presented with significantly reduced corticospinal excitability during the observation of a transitive hand gesture (relative to observation of a static hand) (p < .05), which indicates reduced putative mirror neuron system activity within ventral premotor cortex/inferior frontal gyrus. Among the ASD group, there was also a negative association between putative mirror neuron activity and self-reported social-relating impairments, but there was no indication that mirror neuron impairments in ASD decrease with age.
These data provide general support for the mirror neuron hypothesis of autism; researchers now must clarify the precise functional significance of mirror neurons to truly understand their role in the neuropathophysiology of ASD and to determine whether they should be used as targets for the treatment of ASD.

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    ABSTRACT: Traits of autism spectrum disorder (ASD) in children with attention-deficit/hyperactivity disorder (ADHD) have previously been found to index clinical severity. This study examined the association of ASD traits with diffusion parameters in adolescent males with ADHD (n = 17), and also compared WM microstructure relative to controls (n = 17). Significant associations (p < 0.05, corrected) were found between fractional anisotropy/radial diffusivity and ASD trait severity (positive and negative correlations respectively), mostly in the right posterior limb of the internal capsule/corticospinal tract, right cerebellar peduncle and the midbrain. No case-control differences were found for the diffusion parameters investigated. This is the first report of a WM microstructural signature of autistic traits in ADHD. Thus, even in the absence of full disorder, ASD traits may index a distinctive underlying neurobiology in ADHD.
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    ABSTRACT: The discovery of the mirror neuron system (MNS) is one of the most important neuroscientific achievements in the 20th century. Some researchers had reported that MNS dysfunction was discovered in autism spectrum disorders (ASD). Finally, the 'broken mirror' theory of ASD was announced in the mid 2000's. According to this theory, ASD cannot simulate the mind and behavior of others due to MNS dysfunction; therefore, they cannot imitate the behaviors and empathized with the mind of others. However, ASD does not always show imitation problems. The researchers who have criticized the 'broken mirror' theory proposed the 'social top-down response modulation (STORM)' theory. On STORM theory, the medial prefrontal cortex or temporo-parietal junction, brain areas related with mentalising, might modulate MNS according to social context. We compared the strengths and weaknesses of each theory.
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