Brain Basis for Emotion Recognition Deficits in Depression

There is a emerging understanding of the role of social perception problems in depression and anxiety disorders.  Depression appears to effect the cognitive ability to judge the facial expression of others.  This impairment poses a challenge for interpersonal function and social relationships.  Research is now pinning down the neural basis for this deficit and to determine it’s persistence and the effect of depression remission on this social cognition function.

van Wingen and colleagues from the Netherlands recently published an fMRI study on this topic in Psychological Medicine.  The study had the following elements in research design:

• Subjects: Twenty case subjects with first episode of major depression (medication naive), Twenty one case subjects recovered from a first episode of depression and 30 healthy individuals without a history of depression
• f MRI Task: Visual recognition of anger or fearful face by semantic labelling or visual matching compared to a control task of matching facial orientation without attention to emotion
• Additional Neuropsychological Testing: Depression symptom level, anxiety (state and trait) symptom level, IQ, memory, visual learning, attention, psychomotor speed and executive function.

The depression case subjects were not different from recovered depressed subjects and controls on most of the tests of neuropsychological function.  As expected, they did have higher depression symptom severity scores (Hamilton Depression Scale average for the depressed group was 21.8) and higher anxiety symptom severity scores.

The depressed group performed as well as the remitted group on the control task and the visual emotion matching task.  However, they performed worse than both groups on the semantic matching task, i.e. selecting the correct word label for the emotion displayed visually.  

The brain regions that correlated (increased activation) with impaired semantic emotion labeling included three distinct regions:

• right amygdala
• left inferior frontal gyrus
• anterior cingulate cortex

The authors propose that one explanation for this finding in three distinct brain regions.

“The left inferior frontal gyrus is thought to integrate language with other information (Hagoort, 2005;Willems et al. 2007). Therefore, we suggest that the inferior frontal gyrus may integrate the semantic knowledge about the concepts of anger and fear with the emotional information conveyed by the faces by interacting with the amygdala. The concurrent activation of these systems may subsequently trigger automatic negative thoughts and stimulate task unrelated processes such as rumination (Siegle et al. 2002; Ray et al. 2005), and thereby hinder task appropriate behaviour.”

This explanation fits with the cognitive behavioral theory of depression.  The core concept being that depression is characterized by increased automatic negative thoughts about the self, the future and the environment.  The thoughts are generated by a maladaptive negative cognitive schema.  Activation of these automatic thoughts (i.e. by being shown negative facial emotions) produces distraction from tasks (i.e. correctly labelling these facial emotions). This process appears limited to when depression is present as the recovered depression group showed no deficit.

The authors also conclude the findings could be due to a compensatory mechanism for inadequate behavior or an altered coping mechanism for dealing with demanding situations. 

This study provides additional support that fMRI research may lead to advances in the treatment of depression by both psychotherapy and psychopharmacologic interventions.

Screen shot of 3D Brain showing the limbic system structures amygdala and cingulate cortex (along with the inferior frontal cortex) thought to be involved in impaired facial recogniton in depression.

van Wingen, G., van Eijndhoven, P., Tendolkar, I., Buitelaar, J., Verkes, R., & Fernández, G. (2010). Neural basis of emotion recognition deficits in first-episode major depression Psychological Medicine, 41 (07), 1397-1405 DOI: 10.1017/S0033291710002084