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Meta-analytic evidence of differential prefrontal and early sensory cortex activity during non-social sensory perception in autism.

Accepted version
Peer-reviewed

Type

Article

Change log

Abstract

To date, neuroimaging research has had a limited focus on non-social features of autism. As a result, neurobiological explanations for atypical sensory perception in autism are lacking. To address this, we quantitively condensed findings from the non-social autism fMRI literature in line with the current best practices for neuroimaging meta-analyses. Using activation likelihood estimation (ALE), we conducted a series of robust meta-analyses across 83 experiments from 52 fMRI studies investigating differences between autistic (n = 891) and typical (n = 967) participants. We found that typical controls, compared to autistic people, show greater activity in the prefrontal cortex (BA9, BA10) during perception tasks. More refined analyses revealed that, when compared to typical controls, autistic people show greater recruitment of the extrastriate V2 cortex (BA18) during visual processing. Taken together, these findings contribute to our understanding of current theories of autistic perception, and highlight some of the challenges of cognitive neuroscience research in autism.

Description

Keywords

Activation likelihood estimation (ALE), Autism spectrum conditions, Extrastriate, Meta-analysis, Non-social, Perception, Prefrontal, Sensory processing, V2, fMRI, Autistic Disorder, Humans, Magnetic Resonance Imaging, Neuroimaging, Parietal Lobe, Prefrontal Cortex, Visual Perception

Journal Title

Neurosci Biobehav Rev

Conference Name

Journal ISSN

0149-7634
1873-7528

Volume Title

127

Publisher

Elsevier BV
Sponsorship
Wellcome Trust (214322/Z/18/Z)
NJ was supported by the April Trust PhD Studentship awarded by Newnham College. SBC was funded by the Autism Research Trust, the Wellcome Trust, the Templeton World Charitable Foundation, and the NIHR Biomedical Research Centre in Cambridge, during the period of this work. SBC received funding from the Wellcome Trust 214322\Z\18\Z. For the purpose of Open Access, the author has applied a CC BY public copyright licence to any Author Accepted Manuscript version arising from this submission. Further to this SBC received funding from Innovative Medicines Initiative 2 Joint Undertaking (JU) under grant agreement No 777394. The JU receives support from the European Union's Horizon 2020 research and innovation programme and EFPIA and AUTISM SPEAKS, Autistica, SFARI. SBC also received funding from the Autism Research Trust, Autistica, SFARI, the MRC and the NIHR Cambridge Biomedical Research Centre. The research was supported by the National Institute for Health Research (NIHR) Collaboration for Leadership in Applied Health Research and Care East of England at Cambridgeshire and Peterborough NHS Foundation Trust. The views expressed are those of the author(s) and not necessarily those of the NHS, NIHR or Department of Health and Social Care.