Patients’ judgment of their own mood is unlikely to be accurate; and a subjective assessment is not an ideal diagnostic symptom. Patients with depression typically present with somatic symptoms and, to them, mild depression.1
When seeing their general physician, patients complain of foggy thinking or poor memory and an inability to function properly both at home and at work. “Arguably, it is functional impairment [and not mood] that is the cardinal and most reliable signal of mood disorder,” write Baune, Malhi and Porter in the accompanying editorial. Yet, when a patient is seen by a psychiatrist, how often is cognition per se discussed or examined?
Cognition is rarely given the weight or importance it deserves by psychiatrists.
Consider the checklists psychiatrists use to define mood disorders - where do thought processes and/or cognition feature in these? Typically, psychiatric classification systems consider syndromes – groups of sometimes disparate symptoms that have somehow come together. The authors of the review papers challenge this artificial grouping. One objection is that the symptoms within a syndrome are all given the same weighting, instead of being weighted according to their importance. It seems reasonable to suggest that anhedonia and guilt might count for more in MDD than sleep or appetite disturbance, for example. Similarly, symptoms associated with cognition are not given the weight they deserve.
Unlike psychologists, who consider that mood disorders and depression arise primarily from disorders of thinking, psychiatrists consider them predominantly as disorders of mood. Might psychiatrists, therefore, have to begin to think like psychologists and start considering cognition? Might the question “How do you feel” usefully be re-framed as “How do you think about how you feel?” ask Baune and colleagues.
Most models of mood disorders share the same central components: emotion, cognition and behaviour.
The reviews summarised here and in a further article suggest how the two schools of thought might join heads to better diagnose and manage mood disorders from a cognitive perspective.
Both approaches attempt to explain mood disorder in terms of malfunctioning neural mechanisms. Regardless of the school from which they emanate – psychiatric or psychological models of mood disorders share the same central components: emotion, cognition and behaviour. By studying the neural processes underlying these central components from a neurocognitive perspective, it may be possible to gain a better understanding of each.
Malhi et al. reviewed the literature on prominent neurobiological and neurocognitive models of mood disorder and identify significant similarities.2 Functional neuroimaging is the key investigational tool and its use has underpinned the development of various models of neurocognition in mood disorders. While models may differ significantly, they all describe important cognitive features and deficits that are associated with mood disorders: reappraisal, attention, rumination, reward processing and motivation, response inhibition and impulsivity, and mood stability.
An adaptive cognitive strategy and the basis of CBT, its suppression is associated with memory and cognition deficits. In MDD, reappraisal is diminished compared to healthy controls. This may contribute to the development and maintenance of depressive symptoms.
Attention deployment and control are cognitive strategies that influence and control emotional states and responses. Dysfunctional attentional deployment and control may both be risk factors in MDD
Involuntary self-focusing as a coping mechanism for stress is maladaptive in MDD.
Reward processing and motivation
Anhedonia is widely considered a definitive symptom of MDD and deficits in reward processing are strongly implicated in its aetiology.
Response inhibition, impulsivity and mood stability
These are considered important cognitive deficits in MDD, although more usually associated with bipolar disorder.
If core mood disorder dysfunctions are neurocognitive in origin and treatments can be directly targeted, symptoms are likely to be ameliorated.
The commonality of key cognitive features in depression is all well and good, but how can this help in the clinic? A potential benefit is in improved management. A large body of evidence supports the use of both cognitive behavioural therapy (CBT) and pharmacological therapies in MDD.5,6,7 Interestingly, neuroimaging and the examination of the neural bases underlying the changes associated with each of these therapies have revealed differences in their underlying neural mechanisms. For example, a slower rate of glucose metabolism in the right anterior insula correlates with a better response to CBT, while faster rates correlate with a better response to pharmacological therapies.8 Thus, there is potential for tailoring therapies to particular features of depressed patients.