Neuroimaging

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Neuroimaging

Brain MRI T1 movie.gif

There are have been many differences observed between typically developing children and those with ASD in neuroimaging studies using fMRI, EEG, transcranial magnetic stimulation, EMG, and structural MRI. It has been hypothesized in the Mirror Neuron System Theory of Autism that the social/communication deficits in ASD arise because of differences in activation of the Mirror Neuron System (MNS), since the mirror neuron system plays an integral role in mediating understanding of emotional states of others. However, many different areas of the brain can participate in complex social/communicative tasks, making it difficult to single out just one neural area responsible for the widespread abnormalities in socialization and communication experienced by patients with ASD. Much of current neuroimaging research in ASD operates under one of two different camps that attribute autism to different areas of less activation in the brain.

  1. Theory of Mind-Patients with ASD show lower or no activation in midline structures as compared to a control groups in many tasks, lending credence to the 'Theory Of Mind' explanation for social/communication deficits in patients with ASD. In this theory, patients with ASD have lower activation of mirror neurons in the midline structures which are responsible for "reflecting" about others' emotions or wants1,. Thus, patients have social/communication deficits because they have are unable to process the meaning of other peoples' emotions, which suggests a problem in executive processing.
  2. Embodied Simulation Theory- Scientists who want to test this theory focus their research on shared circuits that are involved in both one's own emotions and other's emotions. Numerous studies have shown that when subjects witness a goal oriented task many different types of neurons are activated in addition to those in the midline structures. For example, when a person watches another person drink a glass of milk with an expression of disgust on his face, the premotor and parietal areas are activated for the action itself, the insula areas are activated in response to the emotion of disgust, and the secondary somatosensory area is activated for the sensations involved in the task. These are the same areas that would have been activated if we drank the milk and were ourselves disgusted. Thus, we are able to understand others' emotional states and intentions because contextual cues activate the same neural circuits that are activated when we perform the same task. However, patients with ASD show diminished activation of these areas as compared to control groups. So, in this theory, the social and communication difficulties arise in patients with ASD because these areas are less activated. Consequently, they have difficulty "understanding" another's actions.1

These two theories are not entirely incompatible and there have been some hypothesis on how the two theories could be integrated to provide a better explanation for the differences seen.

Facial Processing Patients with ASD show less interest in human faces. Normal people perform much better at tasks where they have to identify or match faces that are upright versus inverted. ASD children on the other hand, show a noticeably less pronounced 'inversion effect' as compared to the normal population. Some scientists speculate that this may be because children with ASD process faces similarly to regular objects rather than assigning particular significance to faces, thereby reducing the inversion effect. Another hypothesis is that ASD children may engage more in component processing rather than configural processing, thereby making the activation difference between processing upright faces versus inverted faces smaller. Differences in activation areas are in the frontal cortex and the amygdala, perhaps reflecting a difference in processing the meaning and significance of faces. 2 Typically developing children also seem to activate the right prefrontal areas of the brain when doing self and other face processing while ASD children only activate this area when processing their own face.3

Multi-Voxel Pattern Analysis suggests that although ASD patients can often perform similarly on tasks as control groups, they usually do this through different neurological mechanisms. In one study the prefrontal cortex was imaged and analyzed using MVPA while subjects performed verbal and spacial tasks that may, or may not require the subject to think about another player's state of mind. The group found that there were differences in activation between those with ASD and controls when using MVPA to analyze the fMRI data, but no significant differences in activation if we used convential analysis techniques.7


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