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Understanding altered neural synchrony in first-episode schizophrenia

Published online by Cambridge University Press:  24 June 2014

L (Lea) Williams,
E Gordon,
A Harris,
P Das,
W Wong,
G Flynn,
D Alexander and
T Whitford
L (Lea) Williams
Affiliation:
Brain Dynamics Centre
E Gordon
Affiliation:
Brain Dynamics CentreBrain Resource International Database
A Harris
Affiliation:
Brain Dynamics CentreThe University of Sydney
P Das
Affiliation:
Brain Dynamics CentreNISAD
W Wong
Affiliation:
Brain Dynamics CentreLiverpool Hospital, Sydney, Australia
G Flynn
Affiliation:
Brain Dynamics CentreLiverpool Hospital, Sydney, Australia
D Alexander
Affiliation:
Brain Resource International Database
T Whitford
Affiliation:
Brain Dynamics Centre
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Abstract

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Information

Type
Abstracts from ‘Brainwaves’— The Australasian Society for Psychiatric Research Annual Meeting 2006, 6–8 December, Sydney, Australia
Information
Acta Neuropsychiatrica , Volume 18 , Issue 6 , December 2006, pp. 274 - 275
Copyright
Copyright © 2006 Blackwell Munksgaard

Background:

First-episode schizophrenia (FES) is characterized by psychotic symptoms as well as profound difficulties in cognition and emotion. Our integrative neuroscience model of FES highlights the lack of coordinated neural synchrony underlying these features. The objective was to identify the cognitive, affective and neural synchrony markers that best differentiate FES from healthy controls, and the combination of markers that predict functional outcome.

Methods:

We tested 56 FES (within 3 months of service contact) and 112 matched healthy controls as part of the Brain Resource International Database. Testing included a detailed medical history, psychometric testing, a battery of cognitive tests and EEG recordings in response to cognitive and emotion-related tasks. A new measure of neural synchrony was used to quantify phase synchrony within EEG bands, focusing on gamma.

Results:

FES was defined by marked impairments in social functioning and perceived quality of life, related to severity of negative symptoms. This clinical profile was associated with similarly marked deficits on cognitive measures of executive function, working memory and emotion perception. In terms of neural synchrony, a pattern of ‘hypersynchrony’ compared with healthy controls was apparent in response to processing of salient information.

Conclusions:

These findings provide support for a model of FES that focuses on alterations in synchronization of brain function required for effective binding of complex and significant stimuli. Because poor emotional function and negative symptoms in FES are valid predictors of ‘real-world’ functional outcome, neural synchrony markers show promise as an objective marker of illness progression.