Orienting to social stimuli differentiates social cognitive impairment in autism and schizophrenia
Abstract
Both autism and schizophrenia feature deficits in aspects of social cognition that may be related to amygdala dysfunction, but it is unclear whether these are similar or different patterns of impairment. We compared the visual scanning patterns and emotion judgments of individuals with autism, individuals with schizophrenia and controls on a task well characterized with respect to amygdala functioning. On this task, eye movements of participants are recorded as they assess emotional content within a series of complex social scenes where faces are either included or digitally erased. Results indicated marked abnormalities in visual scanning for both disorders. Controls increased their gaze on face regions when faces were present to a significantly greater degree than both the autism or schizophrenia groups. While the control and the schizophrenia groups oriented to face regions faster when faces were present compared to when they were absent, the autism group oriented at the same rate in both conditions. The schizophrenia group, meanwhile, exhibited a delay in orienting to face regions across both conditions, although whether anti-psychotic medication contributed to this effect is unclear. These findings suggest that while processing emotional information in social scenes, both individuals with autism and individuals with schizophrenia fixate faces less than controls, although only those with autism fail to orient to faces more rapidly based on the presence of facial information. Autism and schizophrenia may therefore share an abnormality in utilizing facial information for assessing emotional content in social scenes, but differ in the ability to seek out socially relevant cues from complex stimuli. Impairments in social orienting are discussed within the context of evidence suggesting the role of the amygdala in orienting to emotionally meaningful information.
Additional Information
© 2007 Elsevier Ltd. Received 21 November 2006, Revised 9 March 2007, Accepted 11 March 2007, Available online 15 March 2007. This project was funded by grants from the National Institutes of Mental Health (STAART grant U54 MH66418; J. Piven), the Cure Autism Now Foundation (R. Adolphs), the National Alliance for Autism Research/Autism Speaks (R. Adolphs), and Johnson and Johnson Pharmaceutical Research and Development, LLC, USA (D. Penn). Noah Sasson was supported by National Institute of Child Health and Human Development Grant T32-HD40127. We are grateful to Monica Stubbs, Ellen Cohen, Morgan Parlier, Shannon Gallagher and Todd Corl for their help collecting and coding these data, Eden Kung for his programming assistance, and Grace Baranek for her help with recruiting participants. We would also like to thank all the individuals who participated in this study.Attached Files
Accepted Version - nihms-25718.pdf
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Additional details
- PMCID
- PMC2128257
- Eprint ID
- 74188
- Resolver ID
- CaltechAUTHORS:20170209-081541468
- U54 MH66418
- NIH
- Cure Autism Now Foundation
- National Alliance for Autism Research
- Johnson and Johnson
- T32-HD40127
- NIH Predoctoral Fellowship
- Autism Speaks
- National Institutes of Mental Health (NIMH)
- National Institute of Child Health and Human Development (NICHD)
- Created
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2017-02-09Created from EPrint's datestamp field
- Updated
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2021-11-11Created from EPrint's last_modified field