Out on Pubmed, from investigators in Glostrup and Copenhagen, Denmark, is this study:Volume of hippocampal subregions and clinical improvement following electroconvulsive therapy in patients with depression.Gbyl K, Rostrup E, Raghava JM, Andersen C, Rosenberg R, Larsson HBW, Videbech P.Prog Neuropsychopharmacol Biol Psychiatry. 2020 Jul 27:110048. doi: 10.1016/j.pnpbp.2020.110048. Online ahead of print.PMID: 32730916 The abstract is copied below:
Abstract
It is thought that the hippocampal neurogenesis is an important mediator of the antidepressant effect of electroconvulsive therapy (ECT). However, most previous studies failed to demonstrate the relationship between the increase in the hippocampal volume and the antidepressant effect. We reinvestigated this relationship by looking at distinct hippocampal subregions and applying repeated measures correlation. Using a 3 Tesla MRI-scanner, we scanned 22 severely depressed in-patients at three time points: before the ECT series, after the series, and at six-month follow-up. The depression severity was assessed by the 17-item Hamilton Rating Scale for Depression (HAMD-17). The hippocampus was segmented into subregions using Freesurfer software. The dentate gyrus (DG) was the primary region of interest (ROI), due to the role of this region in neurogenesis. The other major hippocampal subregions were the secondary ROIs (n = 20). The general linear mixed model and the repeated measures correlation were used for statistical analyses. Immediately after the ECT series, a significant volume increase was present in the right DG (Cohen's d = 1.7) and the left DG (Cohen's d = 1.5), as well as 15 out of 20 secondary ROIs. The clinical improvement, i.e., the decrease in HAMD-17 score, was correlated to the increase in the right DG volume (rrm = -0.77, df = 20, p < .001), and the left DG volume (rrm = -0.75, df = 20, p < .001). Similar correlations were observed in 14 out of 20 secondary ROIs. Thus, ECT induces an increase not only in the volume of the DG, but also in the volume of other major hippocampal subregions. The volumetric increases may reflect a neurobiological process that may be related to the ECT's antidepressant effect. Further investigation of the relationship between hippocampal subregions and the antidepressant effect is warranted. A statistical approach taking the repeated measurements into account should be preferred in the analyses.
And from the text:
Conclusions and implications
A course of ECT induces transient volume increases not only in the DG, but also in several other hippocampal subregions. These volume increases are associated with decreases in the Hamilton scale score, i.e. the clinical improvement. Smaller pre-treatment volumes of several hippocampal subregions, but not the DG, are associated with a better response to ECT.
The study has two main implications: 1) Further investigation of the relationship between the distinct subregions of the hippocampus and the antidepressant effect is warranted. A statistical approach taking the repeated measurements into account should be preferred. Moreover, using T2-weighted data and an ultra-high resolution 7 Tesla scanner could improve the accuracy of the hippocampal subregion segmentation. 2) The predictive value of the smaller pre-treatment hippocampal volumes for the favorable ECT-response should be further investigated. Notably, it is worth assessing whether the combination of the three following types of information yields a sufficient predictive value of favorable ECT-outcome: 1) neuroimaging data described above 2), biochemical tests of the HPA-axis function, and 3) the clinical symptoms of melancholia. Ideally, further investigation should be conducted by initiatives such as the Global ECT-MRI Research Collaboration (Oltedal et al., 2017).
The remarkable structural brain changes associated with ECT have only recently become the focus of intense research scrutiny. The preliminary findings of lack of relationship between structural change and clinical state are now coming into question, with more studies and more sophisticated methodologies, both statistical and imaging. It seems much more intuitive that some of the changes do, in fact, correlate with clinical state.
That the structural changes revert to baseline after months, does not preclude the possibility that they may be due to neurogenesis and are markers of the brain processes necessary to resolve a severe episode of depression.
This is a small study, and the authors' plea for replication with larger cohorts is a an important one.
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