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.

A neurocognitive model for understanding treatment action in depression

“…The presence of emotional biases among patients suffering from depression is well established [11]. Behaviourally, depressed patients show increased processing of negative versus positive emotional information.…”

Cognitive control interventions for depression: A systematic review of findings from training studies

“…At the neuropsychological level, fronto-limbic disruptions are thought to play a crucial role in cognitive impairments involved in emotion regulation (for reviews, see Pizzagalli, 2011;Roiser, Elliott, & Sahakian, 2012). Key findings from neuroimaging studies have shown that depression is associated with disrupted brain activity in the dorsolateral prefrontal cortex (DLPFC) and anterior cingulate cortex (ACC) (Davidson, Pizzagalli, Nitschke, & Putman, 2002;Etkin, Gyurak, & O'Hara, 2013;Pizzagalli, 2011), with decreased activation in these prefrontal areas being related to reduced cognitive control (Collette & Van der Linden, 2002;Smith & Jonides, 1999).…”

Effects of acute transcranial direct current stimulation in hot and cold working memory tasks in healthy and depressed subjects

“…Hypoactivity of the DLPFC and hyperactivity of subcortical structures are associated to MDD and its cognitive deficits [14,18]. Moreover, two modalities of impaired cognitive processing are observed in MDD, namely 'cold' and 'hot' cognition, which refer to information processing in the absence or presence of emotional influence, respectively [19].…”