Abstract
BackgroundCognitive dysfunction is common among depressed patients. However, the pattern and magnitude of impairment during episodes of major depressive disorder (MDD) through to clinical remission remains unclear. Heterogeneity of depressive patients and the lack of longitudinal studies may account for contradictory results in previous research.Methods/DesignThis longitudinal study will analyze cognitive differences between CORE-defined melancholic depressed patients (n = 60) and non-melancholic depressed patients (n = 60). A comprehensive clinical and cognitive assessment will be performed at admission and after 6 months. Cognitive dysfunction in both groups will be longitudinally compared, and the persistence of cognitive impairment after clinical remission will be determined.DiscussionThe study of neuropsychological dysfunction and the cognitive changes through the different phases of depression arise a wide variety of difficulties. Several confounding variables must be controlled to determine if the presence of depression could be considered the only factor accounting for group differences.
Highlights
Cognitive dysfunction is common among depressed patients
The study of neuropsychological dysfunction and the cognitive changes through the different phases of depression arise a wide variety of difficulties
Several confounding variables must be controlled to determine if the presence of depression could be considered the only factor accounting for group differences
Summary
The pattern and magnitude of impairment during episodes of major depressive disorder (MDD) through to clinical remission remains unclear. Heterogeneity of depressive patients and the lack of longitudinal studies may account for contradictory results in previous research. Over the last years cognitive dysfunction has increasingly been recognized as a core feature of major depressive disorder (MDD). Clinical studies have focused on the pattern and magnitude of impairment during and between episodes of MDD as well as the neuropsychological domains affected and the origin of these abnormalities [1]. Results from neuropsychological and neuroimaging studies are still controversial. These contradictory results could be explained mainly by two methodological factors.
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