BMC Psychiatry published an interesting article on the difference between melancholic and non-melancholic depression in terms of cognitive function, and the authors have offered a research design and protocol to test their hypothesis.
It's an open source publication, so the PDF is free to read.
Here is the beginning of the article, offering some definitions and background for the study. Essentially, the authors are proposing that studies on major depression have been flawed in terms of defining subjects. They propose using melancholia ("a disorder with definable clinical signs") which describes a depression in physical symptoms are predominant. This is contrasted by a "reactive or non-melancholic form of depression" which we might generally define as situational or as sadness ("the presence of low mood and tearfulness is frequent and biological markers are not predominant").Melancholic versus non-melancholic depression: differences on cognitive function. A longitudinal study protocol
Saray Monzon
, Margalida Gili
BMC Psychiatry 2010, 10:48doi:10.1186/1471-244X-10-48
Published: 17 June 2010Abstract (provisional)
Background
Cognitive 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
This 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.
Discussion
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.
BackgroundRead the whole paper.
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]. However, results from neuropsychological and neuroimaging studies are still controversial. These contradictory results could be explained mainly by two methodological factors. The first factor is the absence of homogeneity in clinical samples. The heterogeneity of patients evaluated in clinical studies may derive from the different criteria (DSM, ICD) currently used to diagnose MDD and its subtypes. Some authors have pointed out that these criteria poorly identify samples for clinical and outcome studies [2,3]. The second factor explaining controversial results is related to the lack of longitudinal studies that focus on the changes on cognitive function produced through the clinical course of depression. Whether cognitive impairment manifested during periods of depression is long lasting or improves after remission and recovery remains a central issue of study [4]. The cognitive domains affected have neither been clearly identified [5].
To overcome the limitation derived from the first methodological factor, a more accurate selection of depressed patients is required. A pattern of cognitive dysfunction may be more evident in a form of depression characterized by biological markers than in more heterogeneous depressed samples. Melancholia is a disorder with definable clinical signs that identifies more specific populations than the DSM-IV [3]. It describes episodes in which physical symptoms are predominant and is opposed to a reactive or non-melancholic form of depression in which the presence of low mood and tearfulness is frequent and biological markers are not predominant [6].
Overcoming the limitation derived from the lack of longitudinal data imply the development of cohort studies. Longitudinal assessment of cognitive functions seems to be a potentially powerful method of identifying and distinguishing state-related from trait-related cognitive deficits [4]. Previous studies report residual neuropsychological deficits in melancholic patients despite improvement in their depressive symptomatology [7]. Particularly, persisting executive functions and memory disturbances have been observed. This would indicate that some cognitive dysfunction may not be simply secondary to mood disturbances in depression but may represent trait vulnerability markers for MDD. Deficits in other domains of cognitive performance appear to be more state-dependent [8]. The high risk of relapse in depression makes it important to analyze the existence of persisting cognitive impairments during remission, recovery and the euthymic phase of depression. A better understanding of these issues is crucial as it has been suggested that cognitive impairment worsens for every episode of depression and that the observed cognitive impairment in a nonsymptomatic phase of depression may be related to the number of previous episodes [9].
The course of cognitive changes through to clinical improvement in samples of depressed participants with and without melancholia has scarcely been longitudinally studied [6]. The present study aims to analyze longitudinally the cognitive performance of a homogeneous sample of depressed patients. Results of this study can have relevant implications for treatment and neuropsychological rehabilitation.
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