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Multimodal imaging of the mismatch negativity deficit in schizophrenia

Published online by Cambridge University Press:  24 June 2014

R Fulham
Affiliation:
Centre for Brain and Mental Health Studies, Newcastle University
P Michie
Affiliation:
School of Behavioural Sciences, Newcastle University
P Ward
Affiliation:
Schizophrenia Research Unit, Liverpool Hospital, Liverpool, Australia
M Hughes
Affiliation:
Centre for Brain and Mental Health Studies, Newcastle University
U Schall
Affiliation:
Centre for Brain and Mental Health Studies, Newcastle University
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Abstract

Type
Abstracts from ‘Brainwaves’— The Australasian Society for Psychiatric Research Annual Meeting 2006, 6–8 December, Sydney, Australia
Copyright
Copyright © 2006 Blackwell Munksgaard

Background:

Mismatch negativity (MMN) is an elec-trophysiological response to novel auditory stimuli. This project examines the developmental time course of the MMN deficit in schizophrenia and its neurological basis.

Method:

EEG and functional magnetic resonance imaging (fMRI) data were obtained from first-episode and chronic patients with schizophrenia, and matched controls. A duration-deviant MMN paradigm was used in which participants heard an unattended random series of tones consisting of standards (92%, 50 ms) and deviants (8%, 100 ms). High-resolution MMNs were obtained as the difference between deviant and standard ERPs. Cortically constrained LORETA current source density analysis was performed using realistic head models.

Results:

A reduction in MMN amplitude was seen in younger patients (40 years). This is consistent with our previous findings. Current source density analysis of the early phase of the MMN suggests that the major cortical generator of the MMN lies in the superior temporal gyrus (STG) as expected. The latter phase of the MMN engages more anterior cortical regions including premotor cortex. Patients show reduced activity in STG but increased activity in right premotor cortex. fMRI analysis showed that patients have greater activation in the insula and premotor cortex, whereas controls show greater activation in middle frontal gyrus.

Conclusions:

The results are consistent with a deficit that onsets early in the disorder, that is associated with substantially reduced processing within auditory cortex and that leads to different patterns of activation in frontal cortical regions in patients compared with controls.