Autism spectrum disorder (ASD) has historically been characterized by deficits in key areas of social cognition, such as imitation, pragmatic language, theory of mind, and empathy. These behavioral characteristics, which are often difficult to quantify in neurobiological terms, have been increasingly associated with the hypothesis of a dysfunction in the mirror neuron system (ENS). The study by Oberman et al. (2005) provides an important experimental contribution to this hypothesis, using electroencephalography (EEG) to examine the suppression of mu waves—an oscillatory activity in the 8–13 Hz range—as an indirect marker of ENS activation.
The methodology was based on the comparison between individuals with high-functioning ASD and typical controls, both submitted to tasks that involved observing and performing simple manual movements. In neurotypical subjects, suppression of mu activity was evidenced both in the execution and in the observation of movements, suggesting the functional integrity of the mirror neuron system. In individuals with ASD, although there was suppression of mu activity during motor execution, no significant suppression was observed during the observation of another person’s movement – a pattern indicative of specific dysfunction in the observational component of the ENS (Oberman et al., 2005).
This finding has significant implications. Mirror neurons are known to be activated during both the execution and observation of actions, and are considered essential for the construction of internal representations of other people’s actions. Thus, a failure in this system would compromise the ability to mentally map other people’s states and intentions—the neurobiological basis for the deficits in theory of mind and empathy observed in ASD. Furthermore, since the ENS is involved in the association between visual perception and motor programs, its dysfunction could also impair imitation, a skill that is robustly impaired in individuals with autism.
The study also stands out for using a controlled experimental design, including conditions with biological movement (human hand), non-biological movement (bouncing balls) and static visual noise. The absence of mu wave suppression in both groups during the observation of non-biological stimuli reinforces the specificity of the response to intentional movements, which consolidates the use of mu wave suppression as a reliable proxy for ENS activity.
However, the authors acknowledge limitations that are worth highlighting. The sample, composed exclusively of high-functioning men with ASD, limits the generalizability of the findings. Furthermore, the spatial resolution of the EEG does not allow for a precise distinction of the contribution of other regions involved in the observation/execution network, such as the superior temporal sulcus and the inferior parietal cortex, which can also modulate ENS activity. Additionally, although behavioral performance in attention tests was similar between groups, the possibility of different cognitive strategies—such as more analytical or less social attention to the task—cannot be ruled out as a factor influencing the results.
Finally, the authors speculate that the ENS could be involved even in more abstract domains of cognition, such as metaphor comprehension, an area in which individuals with ASD also have difficulties. This proposal suggests that the neural basis of figurative language may be partially based on embodied mechanisms of representation, a promising hypothesis for future investigations.
In summary, the study by Oberman et al. represents robust experimental evidence in favor of the hypothesis of mirror neuron system dysfunction in individuals with ASD. The results point to a potentially unifying neurophysiological substrate of several behavioral symptoms of autism, and at the same time, pave the way for more targeted clinical interventions based on brain biomarkers.
Reference:
OBERMAN, LM et al. EEG evidence for mirror neuron dysfunction in autism spectrum disorders. Cognitive Brain Research, vol. 24, p. 190–198, 2005. DOI: https://doi.org/10.1016/j.cogbrainres.2005.01.014.
