Reward, memory and prediction of treatment response in affective disorders

Abstract

The reward system has been reported to be affected in patients with major depression or anhedonia and has been viewed as a symptom expressed by deficits in experiencing proper reward. In a sample of first-episode and multipleepisode patients with major depression plus healthy controls, Hall et al. [1] for the first time compared functional magnetic resonance imaging (fMRI) during performance of a contingency reversal reward paradigm. They detected group differences in orbitofrontal and medial prefrontal regions. Additionally, nucleus accumbens, anterior cingulate and ventral prefrontal cortices were most activated in healthy controls, less in patients with one-episode and least in multiple-episode patients. Those brain areas may be sensitive to neurobiological alterations during repeated episodes of depression. While impaired cognition and decreased volumes of the hippocampus repeatedly have been reported for patients with major depression, bipolar patients present inconsistent structural imaging data possibly due to lithium therapy. Using a transitive inference (TI) paradigm suitable for assessing relational memory performance and fMRI, Avery et al. [2] examined hippocampal activity and hippocampal volumes via manual segmentation in patients with bipolar disorder compared to healthy controls. They found no differences in any of these parameters between both groups but very well a positive correlation between hippocampal volume and relational memory performance. These results possibly distinguish bipolar disorder from schizophrenia without consulting a common neurogenetic background, which confirms recent genome-wide association studies. Low-resolution brain electromagnetic tomography is a neuroelectric brain imaging technique based on electroencephalography (EEG), which Rentzsch et al. [3] used in combination with assessing symptoms improvement after 4 weeks of antidepressant therapy in patients with major depression to predict treatment response. Responders showed more slow-frequency power in the right anterior cingulate cortex compared to non-responders which the authors attribute to antidepressant treatment response. In a