Abstract
Social perceptual deficits in schizophrenia are well established. Recent work suggests that the ability to extract social information from bodily cues is reduced in patients. However, little is known about the neurobiological mechanisms underlying this deficit. In the current study, 20 schizophrenia patients and 16 controls completed two tasks using point-light animations during fMRI: a basic biological motion task and an emotion in biological motion task. The basic biological motion task was used to localize activity in posterior superior temporal sulcus (pSTS), a critical region for biological motion perception. During the emotion in biological motion task, participants viewed brief videos depicting happiness, fear, anger, or neutral emotions and were asked to decide which emotion was portrayed. Activity in pSTS and amygdala was interrogated during this task. Results indicated that patients showed overall reduced activation compared to controls in pSTS and at a trend level in amygdala across emotions, despite similar task performance. Further, a functional connectivity analysis revealed that controls, but not patients, showed significant positive connectivity between pSTS and left frontal regions as well as bilateral angular gyrus during the emotion in biological motion task. These findings indicate that schizophrenia patients show aberrant neural activity and functional connectivity when extracting complex social information from simple motion stimuli, which may contribute to social perception deficits in this disorder.
| Original language | English |
|---|---|
| Pages (from-to) | 380-387 |
| Number of pages | 8 |
| Journal | NeuroImage: Clinical |
| Volume | 20 |
| DOIs | |
| State | Published - 1 Jan 2018 |
| Externally published | Yes |
Bibliographical note
Publisher Copyright:© 2018 The Authors
Funding
For generous support, we also thank the Brain Mapping Medical Research Organization, Brain Mapping Support Foundation, Pierson-Lovelace Foundation, The Ahmanson Foundation, William M. and Linda R. Dietel Philanthropic Fund at the Northern Piedmont Community Foundation, Tamkin Foundation, Jennifer Jones-Simon Foundation, Capital Group Companies Charitable Foundation, Robson Family, and Northstar Fund. The authors thank Ana Ceci Meyers and Julio Iglesias for assistance in data collection. These data were presented at the 31st annual meeting of the Society for Research in Psychopathology. Funding: This research was supported by the Department of Veterans Affairs Office of Academic Affiliations, Advanced Fellowship Program in Mental Illness Research and Treatment, the VISN 22 Pala pilot grant, and the UCLA Stephen R. Mallory Schizophrenia Research Award. The funders had no role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript.
| Funders | Funder number |
|---|---|
| Advanced Fellowship Program in Mental Illness Research and Treatment | |
| University of California, Los Angeles | |
| Community Foundation | |
| Office of Academic Affiliations, Department of Veterans Affairs |