Prior studies suggest that a dysregulation of the inhibitory neurotransmitter γ-aminobutyric acid (GABA) is involved in the pathophysiology of major depression. We aimed to elucidate changes in cortical GABA content in relation to depression and electroconvulsive therapy (ECT) using magnetic resonance spectroscopy (MRS).

In total, 11 patients with major depression or depressive episode of bipolar disorder (mean pre-ECT Ham-17 of 26) and 11 healthy subjects were recruited. GABA was quantified using short-TE MRS in prefrontal and occipital cortex. Other neurometabolites such as glutathione (GSH), N-acetylaspartate (NAA) and glutamate (Glu) were secondary outcome measures.

No significant differences in GABA/Cr levels were observed between patients at baseline and healthy subjects in prefrontal cortex, t(20)=0.089, p=0.93 or occipital cortex t(21)=0.37, p=0.72. All patients improved on Ham-17 (mean post-ECT Ham-17 of 9). No significant difference was found in GABA, Glu, glutamine, choline or GSH between pre- and post-ECT values. However, we observed a significant decrease in NAA levels following ECT t(22)=3.89, p=0.0038, and a significant correlation between the NAA decline and the number of ECT sessions p=0.035.

Our study does not support prior studies arguing for GABA as a key factor in the treatment effect of ECT on major depression. The reduction in NAA levels following ECT could be due to neuronal loss or a transient dysfunction in prefrontal cortex. As no long-term follow-up scan was performed, it is unknown whether NAA levels will normalise over time.

The prognostic impact of previous depression on myocardial infarction survival remains poorly understood.

To examine the association between depression and all-cause mortality following myocardial infarction.

Using Danish medical registries, we conducted a nationwide population-based cohort study. We included all patients with first-time myocardial infarction (1995–2014) and identified previous depression as either a depression diagnosis or use of antidepressants. We used Cox regression to compute adjusted mortality rate ratios (aMRRs) with 95% confidence intervals.

We identified 170 771 patients with first-time myocardial infarction. Patients with myocardial infarction and a previous depression diagnosis had higher 19-year mortality risks (87% v. 78%). The overall aMRR was 1.11 (95% CI 1.07–1.15) increasing to 1.22 (95% CI 1.17–1.27) when including use of antidepressants in the depression definition.

A history of depression was associated with a moderately increased all-cause mortality following myocardial infarction.

Previous morphology and diffusion-imaging studies have suggested that structural changes in white matter is an important part of the pathophysiology of obsessive–compulsive disorder (OCD). However, different methodological approaches and the heterogeneity of patient samples question the validity of the findings.

In total, 30 patients were matched for age and sex with 30 healthy controls. All participants underwent T1-weighted magnetic resonance imaging, diffusion tensor imaging and T2 fluid-attenuated inversion recovery. Voxel-based morphometry and tract-based spatial statistics were used to compare white matter volumes and diffusion tensor imaging between groups. These data were analysed correcting for the effects of multiple comparisons, age, sex, severity and duration of illness as nuisance covariates. White matter hyperintensities were manually identified.

Increase in fractional anisotropy in cerebellum was the most prominent result. A decrease in fractional anisotrophy in patients comparable with previous studies was located in forceps minor. There were no differences in the white matter morphology or in the white matter hyperintensities between patients and healthy controls.

Decrease in fractional anisotrophy in forceps minor and increase in cerebellum were found, and they were not due to neither white matter hyperintensities nor morphology of the white matter. Cerebellar hyperconnectivity could be an important part of OCD pathophysiology.

The main aim of the present study was to replicate a previous finding in major depressive disorder (MDD) of association between reduced hippocampal volume and the long variant of the di- and triallelic serotonin transporter polymorphism in SLC6A4 on chromosome 17q11.2. Secondarily, we also hypothesised that 5-HTTLPR may be a risk factor for MDD.

Quantitative magnetic resonance imaging (MRI) of the hippocampus was studied in 23 inpatients suffering from MDD and in 33 healthy controls. Normalised volumetric MRI data of hippocampus were assessed with adjustment for total brain volume and tensor-based morphometry was used to elucidate structural brain differences. A triallelic genetic marker resulting from two SLC6A4 promoter region polymorphisms, 5-HTTLPR and rs25531, was analysed for association with MDD and quantitative traits.

Healthy controls had a smaller relative hippocampal volume (relative to brain size) but a larger total brain volume compared with patients with MDD. For patients compared with healthy controls, atrophy was found in the right temporal lobe and pons medulla. Allele and genotype frequencies were strikingly different from the previous study that we aimed to replicate, and no significant associations with the serotonin transporter polymorphism were found.

The present quantitative and morphometric MRI study was not able to replicate the previous finding of association between reduced hippocampal volume in depressed patients and the serotonin transporter polymorphism.

Studies investigating mortality secondary to electroconvulsive therapy (ECT) are few.

To assess the risk of mortality from natural and unnatural causes among ECT recipients compared with other psychiatric in-patients over a 25-year period.

Register-based cohort study of all in-patients admitted to a psychiatric hospital from 1976 to 2000. Cause-specific mortality was analysed using log–linear Poisson regression.

There were 783 deceased in-patients who had received ECT compared with 5781 who had not. Patients who had received ECT had a lower overall mortality rate from natural causes (RR=0.82,95% CI 0.74–0.90) but a slightly higher suicide rate (RR=1.20,95% CI 0.99–1.47), especially within the first 7 days after the last ECT treatment (RR=4.82,95% CI 2.12–10.95).

Further investigation of the effect of ECT on physical health and the observed increased suicide rate immediately following treatment are needed, although the last finding is likely to result from selection bias.