Major depressive disorder (MDD) is characterised by predominately negatively valenced emotional symptoms that are often accompanied by cognitive impairments. We posited that cognitive impairments in MDD are related to altered emotional processing in prefrontal cortex.

We compared 20 medication-free patients with MDD and 29 matched healthy controls. Both groups performed an emotional task during functional magnetic resonance imaging (fMRI). Furthermore, they completed the intra–extra dimensional set shift (IED) test probing for cognitive impairments. Then we correlated the results of the IED with the changes in fMRI BOLD signal in MDD patients and healthy subjects.

The subcategory of the IED applying extradimensional shift (EDS) showed a divergent performance of the MDD group committing significantly more errors than the control group. Correlating the EDS errors with fMRI signal changes, the healthy subjects showed a positive correlation with the right ventrolateral prefrontal cortex and the right orbitofrontal cortex. MDD subjects, in contrast, showed a positive correlation in right dorsolateral prefrontal cortex (DLPFC) and a negative correlation in the left dorsomedial prefrontal cortex (DMPFC).

We hypothesise that the differential correlation in healthy controls and MDD patients may reflect the use of different strategies in their performance. The impaired executive functions, as reflected by altered processing in right DLPFC and left DMPFC, may implicitly influence emotional processing in patients suffering from MDD.

To compare the variability of patterns of depressive symptoms between two consecutive depressive episodes in patients with bipolar disorder type I.

Review of prospectively collected data from 136 subjects of an out-patient bipolar unit from 1997 to 2007. Binomial statistics was used for the analysis of Hamilton Depression Rating Scale (HDRS)-31 items of the first and second episodes, and the correlation of the HDRS-31 item scores of both episodes was determined using the Spearman coefficient.

Ten depressive symptoms showed a significant correlation between index and subsequent episodes: psychological anxiety, somatic anxiety, somatic symptoms, diurnal variation, paranoid symptoms, obsessive and compulsive symptoms, hypersomnia, loss of appetite and helplessness. Only four symptoms were stable in both statistical tests: paranoid symptoms, obsessive–compulsive symptoms, loss of appetite and hypersomnia.

Paranoid and obsessive–compulsive symptoms, loss of appetite and hypersomnia tended to be found in successive episodes. However, the moderate correlations of the symptoms across two depressive recurrences suggested that clinical presentations in bipolar depression may not be predicted by symptom profiles presented in previous episodes.

The present study examined whether low birth weight, prematurity or low birth weight adjusted for gestational age are risk factors for the subsequent development of affective disorder, especially depression.

A population-based case–control design was applied to the Danish Medical Birth Register and the Danish Psychiatric Central Register to identify all individuals born between 1 January 1974 and 31 December 1990 and diagnosed prior to 29 August 2003 with affective disorder alone (ICD-10 F3; 4297 females, 1861 males), schizophrenia alone (ICD-10 F2; 1364 females, 2292 males) or both disorders (ICD-10 F3 + F2; 450 females, 405 males). The association between low birth weight and the risk of developing affective disorder and/or schizophrenia was analysed by conditional logistic regression analysis.

Low birth weight was found to be associated with a significantly elevated risk of developing schizophrenia alone (p = 0.021) and both affective disorder and schizophrenia (p = 0.024), and a non-significantly elevated risk of developing affective disorder alone (p = 0.063). The effect remained significant in the affective disorder and schizophrenia groups (p = 0.039) when correcting for gestational age (premature birth), but was lost in the group with both disorders. Premature birth per se was found to be associated with a significantly elevated risk of developing both affective disorder and schizophrenia (p = 0.00018), an effect that remained significant after adjustment for low birth weight.

Prematurity and low birth weight were found to be risk factors for subsequent development of affective disorder (especially depression) and schizophrenia.

Recently, we reported that mitochondrial respiratory chain complexes I, III and IV were inhibited in the cerebral cortex and cerebellum of rats submitted to chronic mild stress (CMS) and that acute ketamine administration reversed this effect. Therefore, we investigated whether the inhibition of these enzymes may be reversed by chronic administration of ketamine.

Adult male Wistar rats were submitted to CMS and chronically treated with ketamine. After 40 days of CMS, consumption of sweet food, adrenal gland weight, body weight and enzymatic activity of the complexes were measured.

We verified that CMS decreased the intake of sweet food, increased the adrenal gland weight and the control group gained weight after 40 days but the stressed group did not; ketamine administration reversed these effects. We also verified that chronic administration of ketamine reversed the inhibition of complexes I, III and IV in cerebral cortex. However, in cerebellum, only complex IV inhibition was reversed. The chronic ketamine administration partially reverses the inhibition caused by CMS.

We hypothesise that CMS inhibits complexes I, III and IV activities and that chronic administration of ketamine administration partially reverses such an effect. Therefore, it seems reasonable to propose that ketamine administration might be a useful therapy for patients affected by major depression.