Atypical Brain Development

Page by Kyra Mandas and Stephanie Watkins

Since many children with autism show brain growth abnormalities, it has been hypothesized this could be one of the causes. According to Volker and Lopata (2008) an autistic child’s brain goes through an abnormal growth pattern. They begin with an accelerated growth stage right after birth that ends within 24 months and then reaches an exceptionally slow growth period. However, by middle childhood and adolescence their brain size does not differ (Volker & Lopata, 2008). Coskun, Vargheese, Reddoch, Castillo, Pearson, Loveland, Papanicolaou and Sheth (2009) agreed with Volker and Lopata noticing the large brain size at a young age and furthered this by relating it to an autistic child’s over sensitivity to tactile stimuli. They measured the location of receptors to stimuli at different body locations and discovered that the receptors in the brain of a child with autism were spaced father apart. They have hypothesized that because the somatic maps are being formed during this accelerated brain growth that this could be one cause of an autistic child’s extreme sensitivity to sensory input (Coskun, et al., 2008). This is still being researched and currently studies are being conducted examine how impaired social skills in ASD could be caused by atypical organization of the network for imitations in the brain (Shih, Shen, Otti, Keehn, Gaffrey & Muller, 2010).

The broken mirror theory of autism spectrum disorder reflects studies of imitation behavior and the role of mirror neuron regions of the brain. Because individuals diagnosed with autism are known to have great social difficulties, one theory is that damage to the mirror neuron system (MNS) contribute to empathy, language, and theory of mind. Children with autism typically fail imitation tasks of actions or facial expressions in the case that such individuals do not interpret the reasons for imitation. Mirror regions of the brain include the inferior frontal and parietal regions, mostly associated with responding during performance, observation, and imitation (Southgate & Hamilton, 2008). While the relationship between the MNS region of the brain and social difficulties is certainly not causal, it provides another theory about autism’s origin. Below is a visual demonstration of the links between the MNS, behavior, and autism according to the broken mirror theory of autism.

(Southgate & Hamilton, 2008)


Coskun, A.M., Vargheese, L., Reddoch, S., Castillo, E.M., Pearson, D.A., Loveland, K.A., Papanicolaou, A.C., & Sheth, B.R. (2009). How somatic cortical mpas differe in autistic and typical brains. NeuroReport, 20(2), 175-179. doi: 10.1097/WNR.0b013e32831f47d1

Shih, P., Shen, M., Otti, B., Keehn, B., Gaffrey, M.S., &Muller, R. (2010). Atypical network connectivity for imitation in autism spectrum disorder. Developmental Cognitive Neuroscience, 48(10), 2931-2939. doi:10.1016/j.neuropsychologia.2010.05.035

Southgate, V., & Hamilton, A. F. C. (2008). Unbroken mirrors: Challenging a theory of autism. Trends in Cognitive Sciences, 12(6), 225-229.

Volker, M.A., & Lopata, C. (2008). Autism: A review of biological bases, assessment, and intervention. School Psychology Quarterly, 23(2), 258-270. doi: 10.1037/1045-3830.23.2.258


Diagram of MNS, behavior, and autism: Southgate, V., & Hamilton, A. F. C. (2008). Unbroken mirrors: Challenging a theory of autism. Trends in Cognitive Sciences, 12(6), 225-229.

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