Cognitive function and neurocognitive deficits in depression

Impaired cognitions are a recognised feature of major depression. Current research aims to disentangle their specific nature and stability over the disorder’s course, with the distinction between cold (emotionally independent) and hot (emotionally-laden) cognitions providing useful for this purpose. Existing evidence points toward a normal neurocognitive functioning prior to the first depressive episode, with no cold cognitive deficits pre-existing the diagnosis. Higher (pre-)adolescent IQ increases the future likelihood of developing depression, while a trait-like vulnerability is conferred by the hot cognitive tendency to attribute stressful life events to global, stable, and internal causes. In the presence of perceived stress, these negative cognitive styles trigger the depressive episode, characterised by both hot and cold cognitive dysfunctions. Specifically, depression presents as a dysregulation of hot cognition where the individual’s focus on analysing the negative aspects of the environment and the self leads to fewer resources being available for other cognitive processes. This expresses primarily through a state-related cold deficit in psychomotor speed, whereas cold memory deficits progressively install with persistent depression and/or multiple episodes, probably because of state-associated hippocampal changes. Robust evidence indicates that depression has a scarring effect on cold cognitive abilities. While these improve after remission, they do not return to premorbid levels. Moreover, cold deficits in processing speed and long-term memory worsen with every consecutive episode – from negligible after first episode’s remission to large when all recurrences are considered. Depression does not appear to cause a specific scarring to hot cognitions once remission is achieved, although future studies need to ascertain this hypothesis