Autism and the Brain: What Does the Research Say?
Breaking down current theories about autism and the brain.
Posted Mar 07, 2018
For my first few posts on Psychology Today, I wanted to give an overview of the most popular theories about the brain basis of autism. Over the first two blog posts, I'll discuss four theories—but keep in mind there are others as well.
In this first post, I will review the social motivation hypothesis and overly intense world hypothesis.
Social Motivation Hypothesis
One of the core symptoms of autism is a lack of social interaction, especially for young children. Parents often notice that their child with autism is less likely to show them toys or to spontaneously interact with other children or adults compared to neurotypical children.
The social motivation hypothesis proposes that this might be due to the brain’s reward system. We know that for neurotypical individuals, social interactions are rewarding. For example, research has shown that eye contact with attractive faces activates the reward centers of the brain (Kampe, Frith, Dolan, & Frith, 2001). The idea behind the social motivation hypothesis is that maybe children with autism do not find social interactions as rewarding as their neurotypical peers—which would explain why children with autism are less likely to initiate social interaction.
Neuroscience research from my lab (Stavropoulos & Carver, 2014), and others’ (Kohls et al., 2018) have provided evidence for the social motivation hypothesis. We found that children with autism have less reward-related brain activity than their neurotypical peers when they are anticipating social information (Stavropoulos & Carver, 2014).
Even more interesting is how this hypothesis could be extended to better understand restricted interests in autism. Recent research found that children with autism had stronger reward responses to their own restricted interests compared to social rewards (Kohls et al., 2018). Similarly, our group found that children with autism have larger approach and reward related brain activity when anticipating non-social pictures compared to social pictures (Stavropoulos & Carver, 2018).
These findings paint an interesting picture of what might be happening in the brains of children with autism. Maybe restricted interests (such as video games, trains, or cars) are very rewarding, and social interactions are not. It might be the case (although this needs to be studied) that the reward system in autism develops differently than the reward system in neurotypical children, and the reward value of restricted interests (and non-social things) is greater than that of social interactions.
Overly Intense World Hypothesis
Where the social motivation hypothesis focuses only on social behaviors, the overly intense world hypothesis (IWH) talks about both social behavior and sensory symptoms. The IWH says that children with autism might have too much brain activity, which makes it hard to selectively pay attention to some things and not others (Markram, Rinaldi, & Markram, 2007; Markram & Markram, 2010). For example, if you found it difficult to “gate” all the information coming at you while on a conference call at work, it would be difficult to selectively pay attention to one person’s voice and ignore the rest.
It might be similar for children with autism. Maybe children with autism experience the world as overwhelming, and overly intense. That could explain why children with autism often experience sounds as too loud or fabric as too scratchy.
In terms of social behavior, the IWH says that because social interactions are unpredictable and involve a lot of sensory stimulation, children with autism have difficulty and are often overwhelmed by these interactions. This hypothesis has interesting implications for why many children with autism react strongly to various sensations, and why sensory symptoms are so commonly reported by parents and caregivers. It also is a unique theory in that it considers that the root of both social deficits and sensory sensitivity in ASD might be the same: over-responsivity in certain areas of the brain.
The areas of the brain that the IWH says might be over-active include the prefrontal cortex and the amygdala. The prefrontal cortex (sometimes called the neocortex) is where higher-order brain function happens. In this case, higher-order means complex brain functions such as attention, memory, executive function and planning, and social cognition. Some studies show that individuals with autism have hyper-activity (or more activity) in this brain region compared to their typically developing peers (Dichter et al., 2009; Belmonte et al., 2010).
The amygdala is an almond-shaped brain structure that is critical for interpreting and “tagging” emotionally significant things in our environment. For example, if you see a snake and feel a “rush” of fear, you can thank your amygdala. The amygdala has “tagged” snakes as something important (and scary). Similarly, if you hear a song that brings you back to a highly emotional time in your life (such as a hard break-up or your wedding), that’s also your amygdala.
As you might imagine, the amygdala sometimes “tags” things as scary that we wish it didn’t—which is why this brain area has been important to our understanding of anxiety disorders and fear (e.g. Cottraux, 2005). In autism, over-activation in the amygdala is potentially related to why these individuals find social situations unpleasant, or even aversive (Dalton et al., 2005; Kleinhans et al., 2009).
According to the IWH, it might be over-activity of both the prefrontal cortex and amygdala that explains the hyper-sensitivity of individuals on the spectrum. Interestingly, this theory could also explain the exceptional talents of some individuals on the spectrum. For example, individuals with autism may have amazing memories, be able to notice extremely small and important details, or perfect pitch (Pring, 2005).
I hope it was helpful to review and break down these two theories. Stay tuned for the next two in the next post!
Kampe, K.K.W., Frith, C.D., Dolan, R.J., Frith, U. (2001). Reward value of attractiveness and gaze. Nature, 413, 589.
Stavropoulos, K.K.M., & Carver, L.J. (2014). Reward anticipation and processing of social versus nonsocial stimuli in children with and without autism spectrum disorders. Journal of Child Psychology and Psychiatry. dos:10.1111/jcpp.12270.
Kohls, G., Antezana, L., Mosner, M. G., Schultz, R. T., & Yerys, B. E. (2018). Altered reward system reactivity for personalized circumscribed interests in autism. Molecular autism, 9(1), 9.
Stavropoulos, K. K. M., & Carver, L. J. (2018). Oscillatory rhythm of reward: anticipation and processing of rewards in children with and without autism. Molecular autism, 9(1), 4
Markram, K., Rinaldi, T., and Markram, H. (2007b). The intense world syn- drome – an alternative hypothesis for autism. Front. Neurosci. 1:1. doi: 10.3389/neuro.01/1.1.006.2007.
Markram, K., & Markram, H. (2010). The intense world theory–a unifying theory of the neurobiology of autism. Frontiers in human neuroscience, 4, 224.
Dichter, G. S., Felder, J. N., and Bod sh, J. W. (2009). Autism is characterized by dorsal anterior cingulate hyperactivation during social target detection. Soc. Cogn. Affect. Neurosci. 4, 215–226
Belmonte, M. K., Gomot, M., and Baron- Cohen, S. (2010). Visual attention in autism families:“unaffected”sibs share atypical frontal activation. J. Child Psychol. Psychiatry 51, 259–276.
Cottraux, J. (2005). Recent developments in research and treatment for social phobia (social anxiety disorder). Curr. Opin. Psychiatry 18, 51–54.
Dalton, K. M., Nacewicz, B. M., Johnstone, T., Schaefer, H. S., Gernsbacher, M. A., Goldsmith, H. H., Alexander, A. L., and Davidson, R. J. (2005). Gaze fixation and the neural circuitry of face processing in autism. Nat. Neurosci. 8, 519–526.
Kleinhans, N. M., Johnson, L. C., Richards, T., Mahurin, R., Greenson, J., Dawson, G., and Aylward, E. (2009). Reduced neural habituation in the amygdala and social impairments in autism spectrum disorders. Am. J. Psychiatry 166, 467–475.
Pring, L. (2005). Savant talent. Dev. Med. Child Neurol. 47, 500–503.
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