Cognitive mechanisms of treatment in depression

Abstract

Cognitive abnormalities are a core feature of depression, and biases toward negatively toned emotional information are common, but are they a cause or a consequence of depressive symptoms? Here, we propose a 'cognitive neuropsychological' model of depression, suggesting that negative information processing biases have a central causal role in the development of symptoms of depression, and that treatments exert their beneficial effects by abolishing these biases. We review the evidence pertaining to this model: briefly with respect to currently depressed patients, and in more detail with respect to individuals at risk for depression and the effects of antidepressant treatments. As well as being present in currently depressed individuals, negative biases are detectable in those vulnerable for depression due to neuroticism, genetic risk, or previous depressive illness. Recent evidence provides strong support for the notion that both antidepressant drugs and psychological therapies modify negative biases, providing a common mechanism for understanding treatments for depression. Intriguingly, it may even be possible to predict which patients will benefit most from which treatments on the basis of neural responses to negative stimuli. However, further research is required to ascertain whether negative processing biases will be useful in predicting, detecting, and treating depression, and hence in preventing a chronic, relapsing course of illness.

Figure 1

The extended cognitive neuropsychological model of depression. Red boxes indicate factors contributing to the development and maintenance of depressive symptoms. Green boxes indicate factors contributing to the treatment of and recovery from depression. 5-HTTLPR: serotonin transporter-linked polymorphic region.

Figure 2

Hemodynamic responses to negative stimuli in the perigenual anterior cingulate cortex (ACC) predict subsequent response to treatment in depression, but in different directions for pharmacological and psychological treatments. Individuals with greater perigenual ACC responses to negative stimuli have greater mood improvement after treatment with fluoxetine or venlafaxine, whereas the converse is true for responders to cognitive behavioral therapy (CBT) and behavioral activation therapy (BA) (see also DeRubeis et al (2008)). Data redrawn from Chen et al (2007—blue), Davidson et al (2003—red), Dichter et al (2010—yellow), Fu et al (2008—green) and Siegle et al (2006—purple). It must be noted that all studies other than one (Davidson et al, 2003) measured change from baseline in symptoms. Davidson et al (2003) included only symptoms after treatment, but reported that there was no correlation between baseline severity and perigenual ACC response to negative stimuli.