Psychiatric illnesses are often good models for testing the functional relationship between specific regions of the brain. At the same time, one may gain insight into the neurocognitive mechanisms behind a specific disease.
This is the case in a recently published study in Psychiatry Research by Foland et al.:
Evidence for deficient modulation of amygdala response by prefrontal cortex in bipolar mania.
Foland LC, Altshuler LL, Bookheimer SY, Eisenberger N, Townsend J, Thompson PM.
Several studies have implicated the involvement of two major components of emotion regulatory networks, the ventrolateral prefrontal cortex (VLPFC) and amygdala, in the pathophysiology of bipolar disorder. In healthy subjects, the VLPFC has been shown to negatively modulate amygdala response when subjects cognitively evaluate an emotional face by identifying and labeling the emotion it expresses.
The current study used such a paradigm to assess whether the strength of this modulation was altered in bipolar subjects when manic. During functional magnetic resonance imaging (fMRI), nine manic subjects with bipolar I disorder and nine healthy subjects either named the emotion shown in a face by identifying one of two words that correctly expressed the emotion (emotion labeling task) or matched the emotion shown in a face to one of two other faces (emotion perception task). The degree to which the VLPFC regulated amygdala response during these tasks was assessed using a psychophysiological interaction (PPI) analysis.
Compared with healthy subjects, manic patients had a significantly reduced VLPFC regulation of amygdala response during the emotion labeling task. These findings, taken in context with previous fMRI studies of bipolar mania, suggest that reductions in inhibitory frontal activity in these patients may lead to an increased reactivity of the amygdala.
Psychiatry Res. 2008 Jan 15;162(1):27-37.