Article

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: 10.26). 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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    • "Regression analyses showed reduced corticospinal excitability during the observation of transitive hand actions in the ASD group (Enticott et al., 2012). Adapting the experimental design adopted by Fogassi et al. (2005) in humans, Cattaneo et al. (2007) tested with EMG the ability to directly (in a motor way) understand action and intentionality in children with ASD. "
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    ABSTRACT: To understand others’ minds is crucial for survival, however it is quite puzzling how the access to others can be – in some extent – direct and not necessarily mediated by conceptual reasoning. Recent advances in neuroscience have led to hypothesize a role for motor circuits not only in controlling elementary physical features of movement (e.g., force, direction, amplitude), but also in understanding and shaping human behaviour. The concept of motor cognition refers to these aspects, while neurophysiological, neuroimaging, and behavioural studies in human/non-human primates support this view. From a clinical perspective, motor cognition represents a challenge in several domains. A thorough investigation of the neural mechanisms mediating motor action/intention understanding and automatized/compulsive behaviours seems to be a promising way to tackle a range of neurodevelopmental and drug-related disorders. On one hand, anomalies in motor cognition may have cascade effects on social functioning in individuals with Autism Spectrum Disorder (ASD); on the other hand, motor cognition may help to explain the pathophysiology of drug-seeking and drug-taking behaviours in the most severe phase of drug addiction (see, drug dependence, motor low-order cue reactivity). This may represent an essential aspect which could improve the efficacy of rehabilitative interventions. The only way to shed light on multi-factorial disorders such as ASD and drug addiction is through the investigation of their multiple factors. This motor way can promote new theoretical and experimental perspectives that would help to bridge the gap between basic neuroscience approach and clinical practice.
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    • "No group difference in RMT * or response to ppTMS . Enticott et al . , 2012 ASD = 34 M = 26 . 32 One session of single - pulse TMS over M1 * ."
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    • "First, it has been demonstrated that socialcognition is associated with activity in this mirror neuron network in healthy individuals (Baird et al., 2011; Enticott et al., 2008b; Pineda and Hecht, 2009). Secondly, abnormal activation of the mirror system has been demonstrated in schizophrenia (Enticott et al., 2008a; Kato et al., 2011; McCormick et al., 2012; Mehta et al., 2013, 2014; Schurmann et al., 2007) and autism (Dapretto et al., 2006; Enticott et al., 2012; Martineau et al., 2010), although concerns have been raised about consistency of these findings (Dinstein et al., 2010; Hamilton, 2013; Horan et al., 2014; Theoret et al., 2005). Virtual-lesion or transient functional disruption studies (Pascual-Leone et al., 2000) using inhibitory low-frequency magnetic pulses over the inferior frontal gyrus (IFG) (Avenanti et al., 2007; Jacquet and Avenanti, 2013; Keuken et al., 2011) have yielded further clues regarding the spatial and functional properties of this mirror neuron network. "
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