In case we forget - returning to work when depression has remitted

Evidence continues to mount that cognitive impairment is a common and debilitating feature that persists after an episode of acute depression has resolved.

Several recent reviews highlight that the deficits in higher-order cognitive functions and information-processing which may linger in remitted major depressive disorder (MDD) are major factors contributing to poor occupational function and workplace disability when patients return to work.^1,2

Compromising recovery

Psychiatrists are increasingly voicing concerns that more needs to be done to understand and tackle this issue which compromises patient recovery.^2-5  This often over-looked feature of remitted MDD has the potential to hinder both occupational and psychosocial functioning, at a cost to the individual and to society. And the evidence suggests that persistent cognitive deficits are evident from, and maybe before, a first acute episode of major depression, suggesting that cognition-changes may need to be regarded as an integral feature of depression rather than an after-thought.^2,6,7

Function impaired

Meta-analysis of studies in patients with first-episode depression shows that there are significant impairments in psychomotor speed, attention and in most aspects of executive function in patients with remitted MDD  - that is MDD where clinical symptoms have resolved.⁵ Studies suggest that after remission of affective symptoms, people who have experienced MDD perform an average of 0·5–0·7 standard deviations (SDs) lower than the general population on cognitive performance measures.³

This can mean that patients in remission have poorer attention, slowed decision-making, slower information processing and poorer verbal memory than before their depressive episode and when compared with their peers. What is more, there appears to be a subset, of as many as 1 in 5 MDD patients, who experience more severe deficits (greater than 2 SDs from the mean) across several cognitive domains, despite remission of their MDD.⁵  

The social impact of such persistent cognitive deficits is far reaching and clinicians and scientists are waking up to the need to study this phenomenon and finds ways to better measure and manage cognitive impairment in depression. A recently published randomized study (part of the International Study to Predict Optimized Treatment in Depression (iSPOT-D)) adds to the evidence that attention, response inhibition, verbal memory, decision speed and information processing are all impaired even in patients who achieved acute remission of depression after treatment with anti-depressant therapies.⁴  

Cognitive remission as a new goal

Psychiatrists are increasingly referring to these residual and lasting cognitive deficits as indicating an ‘incomplete treatment success’. ⁴ There are calls for clinicians to do more to systematically evaluate and measure cognitive function in people with MDD, using validated tools such as THINC-it® and to start to view the prevention of cognitive impairment – and the achievement of cognitive remission in MDD - as a critical therapeutic priority.²

Patients in remission can have poorer attention, slowed decision-making, slower information processing and poorer verbal memory

Certain patient and clinical factors appear to predict worsened cognitive functional impairment in remitted MDD – such as older age and older age at onset of depression and residual depressive symptoms. ¹ Clinically, there is interest in the emerging evidence suggesting potential differences between antidepressant agents and their impact on cognitive function in MDD.^2,5

Cognitive deficits may predate the onset of clinically significant depressive symptoms,⁵ and whole brain imaging studies in patients with early depression, using functional MRI, suggest that compared with healthy controls, there are early signs of significant abnormalities in key cognition connectivity networks.⁶

Work to be done

Clinicians and scientists are now working in parallel to try to understand the neurobiological underpinning of cognitive functions and areas of overlap with mood regulation, in order to explore putative cognitive-enhancing or preserving effects of potential pharmacological and non-pharmacological interventions.⁵