The Mirror Neuron System In Siblings of Children with An Autism Spectrum Disorder : An EEG Study

Background: The genetic liability for autism spectrum disorder (ASD) is expressed not only as the complete syndrome of autism, but also in milder similar characteristics that have been referred to as the ‘broader autism phenotype’ (BAP). This concept is indicative of the presence of subclinical features that look like characteristics of ASD and which occur more often in first-degree relatives of persons with ASD (Rogers, 2009). Investigating the characteristics of the BAP in relatives of individuals with ASD may provide information concerning the genes underlying this phenotype. In the interest of documenting early manifestations of ASD and its BAP, several researchers investigated siblings of children with ASD.

The discovery of mirror neurons in the macaque brain (Di Pellegrino et al., 1992) and the evidence of a mirror neuron system (MNS) in humans (Keysers & Fadiga, 2008) influenced the interest in the neurobiological processes of ASD. Mirror neuron functioning has been theoretically related to action understanding (Rizzolatti & Craighero, 2004) and various social–communicative functions such as imitation, theory of mind, language and empathy, which are difficulties seen in ASD. However, the findings concerning the role of the MNS in ASD seem controversial and research into the ontogeny of the MNS is inconclusive. Exploring the relationship between mirror neuron functioning and social-communicative functions in ASD may benefit from investigating siblings of children with an ASD.

Objectives: In the interest of systematically documenting early manifestations of ASD and of testing specific hypotheses regarding the ontogeny of the MNS, we conducted an EEG study of high-risk infants, all of whom have an older sibling diagnosed with ASD. Mu suppression is considered to be a good indicator of activity in the MNS (Muthukumaraswamy et al., 2004).

This study had 3 important objectives. First, we have investigated mu wave activity with EEG-recordings during different conditions (age 18 - 30 months). Second, we investigated the relationship between mirror neuron activity and quality of imitation. Finally, we have retested the infants 2,5 years later between the age of 4 and 5 years to investigate the evolution and/or stability of the MNS.

Methods: The experiment consisted of 4 experimental conditions (with 5 different objects) during which brain activity was measured with 64 active electrodes. The infants observed a moving object (object observation condition) and an experimenter performing hand movements (hand movement condition). Subsequently, infants observed (action observation condition) and imitated (action imitation condition) a goal-directed action with each object. Mu wave activity (6-9 Hz) was analysed.

Results: Concerning the first objective, the preliminary results showed no significant difference between mu suppression in the sibling group in comparison with the typical developing control group during all three conditions (age 18 – 30 months).  Full results and conclusions concerning objective 2 and 3 will be presented at the IMFAR meeting.

Conclusions: To our knowledge, the present study is one of the first to investigate mirror neuron activity in young infants at high risk for ASD and may have important implications for further research aimed at understanding neuropsychological processes in ASD.