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Prefrontal cortex function in remitted major depressive disorder

Published online by Cambridge University Press:  01 October 2012

N. L. Nixon*
Affiliation:
Division of Psychiatry, The Institute of Mental Health, University of Nottingham, Nottingham, UK
P. F. Liddle
Affiliation:
Division of Psychiatry, The Institute of Mental Health, University of Nottingham, Nottingham, UK
G. Worwood
Affiliation:
Division of Psychiatry, The Institute of Mental Health, University of Nottingham, Nottingham, UK
M. Liotti
Affiliation:
Department of Psychology, Simon Fraser University, Vancouver, Canada
E. Nixon
Affiliation:
Division of Psychiatry, The Institute of Mental Health, University of Nottingham, Nottingham, UK
*
*Address for correspondence: Dr N. L. Nixon, Division of Psychiatry, The Institute of Mental Health, University of NottinghamInnovation Park, Triumph Road, Nottingham NG7 2TU, UK. (Email: neil.nixon@nottingham.ac.uk)

Abstract

Background

Recent models of major depressive disorder (MDD) have proposed the rostral anterior cingulate (rACC) and dorsomedial prefrontal cortex (dmPFC) as nexus sites in the dysfunctional regulation of cognitive-affective state. Limited evidence from remitted-state MDD supports these theories by suggesting that aberrant neural activity proximal to the rACC and the dmPFC may play a role in vulnerability to recurrence/relapse within this disorder. Here we present a targeted analysis assessing functional activity within these two regions of interest (ROIs) for groups with identified vulnerability to MDD: first, remitted, high predicted recurrence-risk patients; and second, patients suffering observed 1-year recurrence.

Method

Baseline T2* images sensitive to blood oxygen level-dependent (BOLD) contrast were acquired from patients and controls during a Go/No-Go (GNG) task incorporating negative feedback, with 1-year patient follow-up to identify recurrence. BOLD contrast data for error commission (EC) and visual negative feedback (VNF) were used in an ROI analysis based on rACC and dmPFC coordinates from the literature, comparing patients versus controls and recurrence versus non-recurrence versus control groups.

Results

Analysis of patients (n = 20) versus controls (n = 20) showed significant right dmPFC [Brodmann area (BA) 9] hypoactivity within the patient group, co-localized during EC and VNF, with additional significant rACC (BA 32) hypoactivity during EC. The results from the follow-up analysis were undermined by small groups and potential confounders but suggested persistent right dmPFC (BA 9) hypoactivity associated with 1-year recurrence.

Conclusions

Convergent hypoactive right dmPFC (BA 9) processing of VNF and EC, possibly impairing adaptive reappraisal of negative experience, was associated most clearly with clinically predicted vulnerability to MDD.

Type
Original Articles
Copyright
Copyright © Cambridge University Press 2012 

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