Emotion-elicited gamma synchrony in patients with first-episode schizophrenia: a neural correlate of social cognition outcomes

Emotion-elicited gamma synchrony in patients with first-episode schizophrenia: a neural correlate of social cognition outcomes


J Psychiatry Neurosci 2010; 34(4): 303-313

Leanne M. Williams, PhD; Thomas J. Whitford, PhD; Marie Nagy, BSc(Hons); Gary Flynn, MBBS; Anthony W.F. Harris, PhD; Steven M. Silverstein, PhD; Evian Gordon, PhD, MBBS

Williams, Whitford, Nagy, Flynn, Harris, Gordon — Brain Dynamics Centre, Westmead Millennium Institute and Western Clinical School, University of Sydney, Westmead Hospital; Williams, Harris, Gordon — Discipline of Psychological Medicine, Faculty of Medicine, University of Sydney; Silverstein — University of Medicine and Dentistry, New Jersey; Gordon — Brain Resource International Database, Brain Resource headquarters, Sydney, Australia.


Background: Schizophrenia may be understood as a disorder of neural synchrony. There is also increasing evidence that emotional and social cognitive impairments are central to this disorder. In patients with first-episode schizophrenia, we examined whether emotion perception is associated with disruptions to high-frequency (40 Hz) gamma synchrony and whether these disruptions predict selfregulatory adaptive compensations reflected in social cognitive behaviours.

Methods: We obtained electroencephalography recordings from 28 patients with first-episode schizophrenia and matched healthy controls during perception of facial emotion under both conscious and nonconscious conditions. We extracted gamma-band synchrony from the electroencephalogram. We also used behavioural measures of emotion identification, emotional intelligence, negativity bias and social function, along with ratings of first-episode schizophrenia symptoms. We analyzed group differences and predicted social cognition to assess the potential contribution of medication.

Results: Within 200 ms poststimulus, patients with first-episode schizophrenia showed alterations in gamma synchrony during both conscious and nonconscious emotion perception. Stimulus-locked synchrony was reduced in patients, particularly over the temporal cortex, whereas complementary enhancements in absolute gamma synchrony (independent of stimuli) were more distributed over temporal and left parieto-occipital regions. This pattern of altered synchrony predicted poor performance on each measure of social cognition among these patients. Medication dosage did not correlate significantly with either gamma synchrony or behavioural measures in this group.

Limitations: Limitations to our study include the lack of comparison between medicated and unmedicated patients or between types of medication.

Conclusions: These findings suggest that disruptions in integrative processing of motivationally important stimuli show promise as a potential biological marker of social cognitive impairments, present from the first episode of schizophrenia, and their outcomes.

The study was conducted at The Brain Dynamics Centre, Westmead Hospital and University of Sydney, NSW, 2006, Australia.

Submitted Jul. 2, 2008; Revised Jul. 4, Oct. 6, 2008, Jan. 4, 2009; Accepted Jan. 6, 2009

Acknowledgements: Dr. Williams holds a peer-reviewed Pfizer Foundation Senior Research Fellowship, which supported this study. Dr. Whitford was supported by this fellowship in a postdoctoral position. We acknowledge the support of the Brain Resource International Database (under the auspices of Brain Resource; www .brainresource.com) for collaboration in data acquisition. All scientific decisions are made independent of BR operations via the independently operated scientific division, BRAINnet (www.brainnet .net), which is overseen by the independently funded Brain Dynamics Centre and scientist members.

Competing interests: None declared for Drs. Whitford, Nagy and Flynn. Dr. Williams is a minor shareholder (< 1%) in Brain Resource and has received fees from them for work unrelated to this study. Dr. Harris has received speaker fees from Janssen-Cilag Australia, Bristol Myers Squibb and CME LLC and travel assistance from Janssen-Cilag Australia. Dr. Silverstein has received fees from Brain Resource for work unrelated to this study. Dr. Gordon is CEO of Brain Resource, with significant financial interest in company. Note, however, that scientific decisions about research and publication using the Brain Resource International Database are made by a scientific network (Brain Research and Integrative Neuroscience Network, BRAINnet; see www.brainnet.net),which is independently administered via a peer-review process. Brain Resource had no direct involvement in the design and implementation of the project. Contributors: Drs. Williams and Gordon designed the study. Drs. Whitford, Flynn and Harris acquired the data, which Drs. Williams, Whitford, Nagy, Flynn, Silverstein and Gordon analyzed. Drs. Williams and Gordon wrote the article. All authors reviewed the article and approved it final publication

Correspondence to: Dr. L.M. Williams, The Brain Dynamics Centre, Acacia House, Westmead Hospital, Westmead NSW, 2145, Australia; fax 61 2 9635 7734; lea_williams@wmi.usyd.edu.au