Background
Altered cognitive processing following mood challenge is associated with elevated
relapse risk in remitted unipolar depressed patients, but little is known about the
neural basis of this reactivity and its link to depressive relapse and prophylaxis.
Methods
Remitted unipolar depressed participants (n = 16) and healthy control subjects (n = 16) underwent functional magnetic resonance imaging (fMRI) while viewing sad and
neutral film clips. Correlations were determined between emotional reactivity (neural
responses to sad vs. neutral films) in remitted patients and subsequent relapse status
over an 18 month follow-up period. A receiver operating characteristic analysis was
used to determine signal cutoffs for predicting relapse. Emotional reactivity in relapse
prognostic areas was compared between groups.
Results
Within the remitted group, relapse was predicted by medial prefrontal cortical (mPFC;
Brodmann's area 32) activity and contraindicated by visual cortical activity (Brodmann's
area 17). mPFC reactivity predicted rumination, whereas visual cortical reactivity
predicted distress tolerance (acceptance). Compared with control participants, remitted
depressed patients demonstrated a more pronounced tradeoff between mPFC and visual
cortex reactivity. The difference score between mPFC and visual reactivity yielded
excellent prediction of depressive relapse.
Conclusions
Medial prefrontal cortical reactivity to mood provocation in remitted unipolar depressed
patients serves as a marker of relapse risk rather than successful emotion regulation.
Enduring remission is characterized by normalization of the mPFC to that of healthy
control subjects. Furthermore, visual cortex reactivity predicts resilience against
depressive relapse, indicating a prophylactic role for sensory rather than ruminative
cognitive reactivity in the processing of negative emotion.
Key Words
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Article info
Publication history
Published online: May 02, 2011
Accepted:
March 5,
2011
Received in revised form:
February 12,
2011
Received:
December 1,
2010
Identification
Copyright
© 2011 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.
