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Carlisi, C. O., Norman, L., Murphy, C. M., Christakou, A. 
ORCID: https://orcid.org/0000-0002-4267-3436, Chantiluke, K., Giampietro, V., Simmons, A., Brammer, M., Murphy, D. G., MRC, A. C., Mataix-Cols, D. and Rubia, K.
(2016)
Disorder-specific and shared brain abnormalities during vigilance in autism and obsessive-compulsive disorder.
Biological Psychiatry.
ISSN 0006-3223
doi: 10.1016/j.bpsc.2016.12.005
Abstract/Summary
Background Autism spectrum disorder (ASD) and obsessive-compulsive disorder (OCD) are often comorbid and share similarities across some cognitive phenotypes, including certain aspects of attention. However, no functional magnetic resonance imaging (fMRI) studies have compared the underlying neural mechanisms contributing to these shared phenotypes. Methods Age and IQ-matched boys between 11 and 17 years old with ASD (N=20), OCD (N=20) and healthy controls (N = 20) performed a parametrically modulated psychomotor vigilance fMRI task. Brain activation and performance were compared between adolescents with OCD, ASD and controls. Results While boys with ASD and OCD were not impaired on task performance, there was a significant group by attention load interaction in several brain regions. With increasing attention load, left inferior frontal cortex/insula as well as left inferior parietal lobe/pre/post-central gyrus were progressively less activated in OCD boys relative to the other two groups. In addition, OCD boys showed progressively increased activation with increasing attention load in rostromedial prefrontal/anterior cingulate cortex relative to ASD and control boys. Shared neurofunctional abnormalities between ASD and OCD boys included increased activation with increasing attention load in cerebellum and occipital regions, possibly reflecting increased default mode network activation. Conclusions This first fMRI study to compare boys with ASD and OCD showed shared abnormalities in posterior cerebellar-occipital brain regions. However, OCD boys showed a disorder-specific pattern of reduced activation in left inferior frontal and temporo-parietal regions but increased activation of medial frontal regions which may potentially be related to neurobiological mechanisms underlying cognitive and clinical phenotypes of OCD.
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