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Depression: Breakdown Of Normal Emotional Processing?

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Brain imaging has revealed a breakdown in normal patterns of emotional processing that impairs the ability of people with clinical depression to suppress negative emotional states. Efforts by depressed patients to suppress their feelings when viewing emotionally negative images enhanced activity in several brain areas, including the amygdala, known to play a role in generating emotion.

“Identifying areas in the nervous system that correlate to pathological mood states is one of the pressing questions in mental illness today,” says Carol Tamminga, MD, of the University of Texas Southwest Medical Center. Tamminga was not involved in the study.

Tom Johnstone, PhD, of the University of Wisconsin, and colleagues there and at Tufts University studied 21 adults diagnosed with major depressive disorder and 18 healthy subjects of comparable ages. Participants were asked to view a series of emotionally positive and negative images and then indicate their reaction to each one. Four seconds after the presentation of each picture, participants were asked either to increase their emotional response (for example, imagining a loved one experiencing what was depicted in the image), to decrease it, or simply to continue watching the image.

During the test, a functional magnetic resonance imaging scanner detected changes in neural activity. Johnstone and his colleagues also recorded levels of emotional excitement by measuring pupil dilation.

The data showed distinctive patterns of activity in the ventromedial prefrontal cortex (VMPFC) and the right prefrontal cortex (PFC), areas that regulate the emotional output generated from the amygdala. The VMPFC is compromised in depression, likely because of the inappropriate engagement of right PFC circuitry in depressed individuals.

“These findings underscore the importance of emotional regulation deficits in depression,” says Johnstone. “They also suggest targets for therapeutic intervention.”

According to previous research, normal interaction between the amygdala and the VMPFC may underlie the proper adaptation of levels of the stress hormone cortisol on a daily basis. These levels do not vary as widely in people with major depressive disorder; future research may now be able to clarify the mechanism that underlies this aspect of depression. It could also examine the possibility of using measurements of activity in the amygdala to predict the effectiveness of treatments for depression such as cognitive behavioral therapy.

J Neurosci. 2007 Aug 15;27(33):8877-84.

Failure to regulate: counterproductive recruitment of top-down prefrontal-subcortical circuitry in major depression.

Johnstone T, van Reekum CM, Urry HL, Kalin NH, Davidson RJ.

Waisman Laboratory for Brain Imaging and Behavior, University of Wisconsin-Madison, Madison, Wisconsin 53705, USA. itjohnstone@wisc.edu

Although depressed mood is a normal occurrence in response to adversity in all individuals, what distinguishes those who are vulnerable to major depressive disorder (MDD) is their inability to effectively regulate negative mood when it arises. Investigating the neural underpinnings of adaptive emotion regulation and the extent to which such processes are compromised in MDD may be helpful in understanding the pathophysiology of depression. We report results from a functional magnetic resonance imaging study demonstrating left-lateralized activation in the prefrontal cortex (PFC) when downregulating negative affect in nondepressed individuals, whereas depressed individuals showed bilateral PFC activation. Furthermore, during an effortful affective reappraisal task, nondepressed individuals showed an inverse relationship between activation in left ventrolateral PFC and the amygdala that is mediated by the ventromedial PFC (VMPFC). No such relationship was found for depressed individuals, who instead show a positive association between VMPFC and amygdala. Pupil dilation data suggest that those depressed patients who expend more effort to reappraise negative stimuli are characterized by accentuated activation in the amygdala, insula, and thalamus, whereas nondepressed individuals exhibit the opposite pattern. These findings indicate that a key feature underlying the pathophysiology of major depression is the counterproductive engagement of right prefrontal cortex and the lack of engagement of left lateral-ventromedial prefrontal circuitry important for the downregulation of amygdala responses to negative stimuli.

PMID: 17699669 [PubMed – in process]

Written by huehueteotl

August 21, 2007 at 3:53 pm

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