Increased resting‐state thalamocortical functional connectivity in children and young adults with autism spectrum disorder.

There is converging evidence that abnormal thalamocortical interactions contribute to attention deficits and sensory sensitivities in autism spectrum disorder (ASD). However, previous functional MRI studies of thalamocortical connectivity in ASD have produced inconsistent findings in terms of both the direction (hyper vs. hypoconnectivity) and location of group differences. This may reflect, in part, the confounding effects of head motion during scans. In the present study, we investigated resting‐state thalamocortical functional connectivity in 8–25 year‐olds with ASD and their typically developing (TD) peers. We used pre‐scan training, on‐line motion correction, and rigorous data quality assurance protocols to minimize motion confounds. ASD participants showed increased thalamic connectivity with temporal cortex relative to TD. Both groups showed similar age‐related decreases in thalamic connectivity with occipital cortex, consistent with a process of circuit refinement. Findings of thalamocortical hyperconnectivity in ASD are consistent with other evidence that decreased thalamic inhibition leads to increase and less filtered sensory information reaching the cortex where it disrupts attention and contributes to sensory sensitivity. This literature motivates studies of mechanisms, functional consequences, and treatment of thalamocortical circuit dysfunction in ASD. Lay Summary: The thalamus is a deep brain structure that receives information from the senses and amplifies or inhibits its relay to the cortex via thalamocortical circuits. Using functional brain imaging, we found increased communication between the thalamus and specific cortical regions in children and young adults with autism spectrum disorder (ASD) compared with their typically developing peers. We hypothesize that increased thalamocortical communication in ASD reflects reduced thalamic inhibition of irrelevant sensory information from being relayed to the cortex, and contributes to attention deficits and sensory sensitivities. [ABSTRACT FROM AUTHOR]