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Increased neural response to fear in patients recovered from depression: a 3T functional magnetic resonance imaging study

Published online by Cambridge University Press:  23 July 2009

R. Norbury*
Affiliation:
Psychopharmacology Research Unit (PPRU), University of Oxford, Department of Psychiatry, Oxford, UK
S. Selvaraj
Affiliation:
Psychopharmacology Research Unit (PPRU), University of Oxford, Department of Psychiatry, Oxford, UK
M. J. Taylor
Affiliation:
Psychopharmacology Research Unit (PPRU), University of Oxford, Department of Psychiatry, Oxford, UK
C. Harmer
Affiliation:
Psychopharmacology and Emotion Research Laboratory (PERL), University of Oxford, Department of Psychiatry, Oxford, UK
P. J. Cowen
Affiliation:
Psychopharmacology Research Unit (PPRU), University of Oxford, Department of Psychiatry, Oxford, UK
*
*Address for correspondence: Dr R. Norbury, Psychopharmacology Research Unit (PPRU), University of Oxford, Department of Psychiatry, Neurosciences Building, Warneford Hospital, Headington, OxfordOX3 7JX, UK. (Email: raymond.norbury@psych.ox.ac.uk)

Abstract

Background

Previous imaging studies have revealed that acute major depression is characterized by altered neural responses to negative emotional stimuli. Typically, responses in limbic regions such as the amygdala are increased while activity in cortical regulatory regions such as the dorsolateral prefrontal cortex (DLPFC) is diminished. Whether these changes persist in unmedicated recovered patients is unclear.

Method

We used functional magnetic resonance imaging to examine neural responses to emotional faces in a facial expression-matching task in 16 unmedicated recovered depressed patients and 21 healthy controls.

Results

Compared with controls, recovered depressed patients had increased responses bilaterally to fearful faces in the DLPFC and right caudate. Responses in the amygdala did not distinguish the groups.

Conclusions

Our findings indicate that clinical recovery from depression is associated with increased activity in the DLPFC to negative emotional stimuli. We suggest that this increase may reflect a compensatory cortical control mechanism with the effect of limiting emotional dysregulation in limbic regions such as the amygdala.

Type
Original Articles
Copyright
Copyright © Cambridge University Press 2009

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