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Published Online: 1 August 2012

Regional fMRI Hypoactivation and Altered Functional Connectivity During Emotion Processing in Nonmedicated Depressed Patients With Bipolar II Disorder

Nathalie Vizueta, Ph.D., Jeffrey D. Rudie, Ph.D., Jennifer D. Townsend, B.A., Salvatore Torrisi, M.A., Teena D. Moody, Ph.D., Susan Y. Bookheimer, Ph.D., and Lori L. Altshuler, M.D.Authors Info & Affiliations
Publication: American Journal of Psychiatry
Volume 169, Number 8
https://doi.org/10.1176/appi.ajp.2012.11030349
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Abstract

Objective:

Although the amygdala and ventrolateral prefrontal cortex have been implicated in the pathophysiology of bipolar I disorder, the neural mechanisms underlying bipolar II disorder remain unknown. The authors examined neural activity in response to negative emotional faces during an emotion perception task that reliably activates emotion regulatory regions.

Method:

Twenty-one nonmedicated depressed bipolar II patients and 21 healthy comparison subjects underwent functional MRI (fMRI) while performing an emotional face-matching task. Within- and between-group whole-brain fMRI activation and seed-based connectivity analyses were conducted.

Results:

In depressed bipolar II patients, random-effects between-group fMRI analyses revealed a significant reduction in activation in several regions, including the left and right ventrolateral prefrontal cortices (Brodmann's area [BA] 47) and the right amygdala, a priori regions of interest. Additionally, bipolar patients exhibited significantly reduced negative functional connectivity between the right amygdala and the right orbitofrontal cortex (BA 10) as well as the right dorsolateral prefrontal cortex (BA 46) relative to healthy comparison subjects.

Conclusions:

These findings suggest that bipolar II depression is characterized by reduced regional orbitofrontal and limbic activation and altered connectivity in a fronto-temporal circuit implicated in working memory and emotional learning. While the amygdala hypoactivation observed in bipolar II depression is opposite to the direction seen in bipolar I mania and may therefore be state dependent, the observed orbitofrontal cortex hypoactivation is consistent with findings in bipolar I depression, mania, and euthymia, suggesting a physiologic trait marker of the disorder.

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Information & Authors

Information

Published In

Go to American Journal of Psychiatry
Go to American Journal of Psychiatry
American Journal of Psychiatry
Volume 169 • Number 8 • August 2012
Pages: 831 - 840
PubMed: 22773540

History

Received: 2 March 2011
Revision received: 12 September 2011
Revision received: 19 February 2012
Accepted: 16 March 2012
Published online: 1 August 2012
Published in print: August 2012

Authors

Affiliations

Nathalie Vizueta, Ph.D.
From the Semel Institute for Neuroscience and Human Behavior, the Department of Psychiatry and Biobehavioral Sciences, and the Ahmanson-Lovelace Brain Mapping Center and Neuroscience Interdepartmental Program, David Geffen School of Medicine, University of California, Los Angeles; and the Department of Psychiatry, VA Greater Los Angeles Healthcare System, West Los Angeles Healthcare Center, Los Angeles.
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Jeffrey D. Rudie, Ph.D.
From the Semel Institute for Neuroscience and Human Behavior, the Department of Psychiatry and Biobehavioral Sciences, and the Ahmanson-Lovelace Brain Mapping Center and Neuroscience Interdepartmental Program, David Geffen School of Medicine, University of California, Los Angeles; and the Department of Psychiatry, VA Greater Los Angeles Healthcare System, West Los Angeles Healthcare Center, Los Angeles.
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Jennifer D. Townsend, B.A.
From the Semel Institute for Neuroscience and Human Behavior, the Department of Psychiatry and Biobehavioral Sciences, and the Ahmanson-Lovelace Brain Mapping Center and Neuroscience Interdepartmental Program, David Geffen School of Medicine, University of California, Los Angeles; and the Department of Psychiatry, VA Greater Los Angeles Healthcare System, West Los Angeles Healthcare Center, Los Angeles.
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Salvatore Torrisi, M.A.
From the Semel Institute for Neuroscience and Human Behavior, the Department of Psychiatry and Biobehavioral Sciences, and the Ahmanson-Lovelace Brain Mapping Center and Neuroscience Interdepartmental Program, David Geffen School of Medicine, University of California, Los Angeles; and the Department of Psychiatry, VA Greater Los Angeles Healthcare System, West Los Angeles Healthcare Center, Los Angeles.
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Teena D. Moody, Ph.D.
From the Semel Institute for Neuroscience and Human Behavior, the Department of Psychiatry and Biobehavioral Sciences, and the Ahmanson-Lovelace Brain Mapping Center and Neuroscience Interdepartmental Program, David Geffen School of Medicine, University of California, Los Angeles; and the Department of Psychiatry, VA Greater Los Angeles Healthcare System, West Los Angeles Healthcare Center, Los Angeles.
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Susan Y. Bookheimer, Ph.D.
From the Semel Institute for Neuroscience and Human Behavior, the Department of Psychiatry and Biobehavioral Sciences, and the Ahmanson-Lovelace Brain Mapping Center and Neuroscience Interdepartmental Program, David Geffen School of Medicine, University of California, Los Angeles; and the Department of Psychiatry, VA Greater Los Angeles Healthcare System, West Los Angeles Healthcare Center, Los Angeles.
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Lori L. Altshuler, M.D.
From the Semel Institute for Neuroscience and Human Behavior, the Department of Psychiatry and Biobehavioral Sciences, and the Ahmanson-Lovelace Brain Mapping Center and Neuroscience Interdepartmental Program, David Geffen School of Medicine, University of California, Los Angeles; and the Department of Psychiatry, VA Greater Los Angeles Healthcare System, West Los Angeles Healthcare Center, Los Angeles.
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Notes

Address correspondence to Dr. Vizueta ([email protected]).

Funding Information

Dr. Altshuler has served on the advisory boards or speakers bureaus of Forest Laboratories, Merck, and Sepracor and has served as a consultant to Eli Lilly. All other authors report no financial relationships with commercial interests.Supported by NIMH grants (K24 MH-01848, T32 MH-17140) and a fellowship from the University of California, Los Angeles, Integrative Study Center in Mood Disorders to Dr. Vizueta; by grants from the National Center for Research Resources (RR12169, RR13642, and RR00865); and by the Ahmanson Foundation, the Brain Mapping Medical Research Organization, the Brain Mapping Support Foundation, the Capital Group Companies Charitable Foundation, the Jennifer Jones-Simon Foundation, the Northstar Fund, the Pierson-Lovelace Foundation, the Robson Family, the Tamkin Foundation, and the William M. and Linda R. Dietel Philanthropic Fund at the Northern Piedmont Community Foundation.

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