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      Effect of electroconvulsive therapy on hippocampal and amygdala volumes: systematic review and meta-analysis

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          Abstract

          Background

          Electroconvulsive therapy (ECT) is one of the most effective treatments for depression, although the underlying mechanisms remain unclear. Animal studies have shown that electroconvulsive shock induced neuroplastic changes in the hippocampus.

          Aims

          To summarise volumetric magnetic resonance imaging studies investigating the effects of ECT on limbic brain structures.

          Method

          A systematic review and meta-analysis was conducted to assess volumetric changes of each side of the hippocampus and amygdala before and after ECT. Standardised mean difference (SMD) was calculated.

          Results

          A total of 8 studies ( n = 193) were selected for our analyses. Both right and left hippocampal and amygdala volumes increased after ECT. Meta-regression analyses revealed that age, percentage of those responding and percentage of those in remission were negatively associated with volume increases in the left hippocampus.

          Conclusions

          ECT increased brain volume in the limbic structures. The clinical relevance of volume increase needs further investigation.

          Declaration of interest

          None.

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          Most cited references54

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          Chronic antidepressant treatment increases neurogenesis in adult rat hippocampus.

          Eric J. Nestler, J Malberg, Amelia J. Eisch … (2000)
          Recent studies suggest that stress-induced atrophy and loss of hippocampal neurons may contribute to the pathophysiology of depression. The aim of this study was to investigate the effect of antidepressants on hippocampal neurogenesis in the adult rat, using the thymidine analog bromodeoxyuridine (BrdU) as a marker for dividing cells. Our studies demonstrate that chronic antidepressant treatment significantly increases the number of BrdU-labeled cells in the dentate gyrus and hilus of the hippocampus. Administration of several different classes of antidepressant, but not non-antidepressant, agents was found to increase BrdU-labeled cell number, indicating that this is a common and selective action of antidepressants. In addition, upregulation of the number of BrdU-labeled cells is observed after chronic, but not acute, treatment, consistent with the time course for the therapeutic action of antidepressants. Additional studies demonstrated that antidepressant treatment increases the proliferation of hippocampal cells and that these new cells mature and become neurons, as determined by triple labeling for BrdU and neuronal- or glial-specific markers. These findings raise the possibility that increased cell proliferation and increased neuronal number may be a mechanism by which antidepressant treatment overcomes the stress-induced atrophy and loss of hippocampal neurons and may contribute to the therapeutic actions of antidepressant treatment.
          Article 0 comments Cited 342 times – based on 0 reviews     Review now
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            Hippocampal granule neuron number and dentate gyrus volume in antidepressant-treated and untreated major depression.

            Maura Boldrini, Adrienne Santiago, Rene Hen … (2013)
            Smaller hippocampal volume is reported in major depressive disorder (MDD). We hypothesize that it may be related to fewer granule neurons (GN) in the dentate gyrus (DG), a defect possibly reversible with antidepressants. We studied age-, sex-, and postmortem interval-matched groups: no major psychopathology (controls); unmedicated-MDD; and MDD treated with serotonin reuptake inhibitors (MDD*SSRI) or tricyclics (MDD*TCA). Frozen right hippocampi were fixed, sectioned (50 μm), immunostained with neuronal nuclear marker (NeuN), and counterstained with hematoxylin. GN and glial number, and DG and granule cell layer (GCL) volumes were stereologically estimated. Fewer GNs in the anterior DG were present in unmedicated-MDDs compared with controls (p=0.013). Younger age of MDD onset correlated with fewer GNs (p=0.021). Unmedicated-MDDs had fewer mid-DG GNs than MDD*SSRIs (p=0.028) and controls (p=0.032). Anterior GCL glial number did not differ between groups. Anterior/mid GCL volume was smaller in unmedicated-MDDs vs controls (p=0.008) and larger in MDD*SSRIs vs unmedicated-MDDs (p<0.001), MDD*TCAs (p<0.001), and controls (p<0.001). Anterior GCL volume and GN number (r=0.594, p=0.001), and mid DG volume and GN number (r=0.398, p=0.044) were correlated. Anterior DG capillary density correlated with GN number (p=0.027), and with GCL (p=0.024) and DG (r=0.400, p=0.047) volumes. Posterior DG volume and GN number did not differ between groups. Fewer GNs in unmedicated-MDD without fewer neuronal progenitor cells, as previously reported, suggests a cell maturation or survival defect, perhaps related to MDD duration. This may contribute to a smaller hippocampus and is potentially reversed by SSRIs. Postmortem studies are correlative and animal studies are needed to test implied causal relationships.
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              Efficacy of ECT in depression: a meta-analytic review.

              Daniel Pagnin, Stefano Pini, Giovanni Battista Cassano … (2004)
              This study analyzed the efficacy of electroconvulsive therapy (ECT) in depression by means a meta-analytic review of randomized controlled trials that compared ECT with simulated ECT or placebo or antidepressant drugs and by a complementary meta-analytic review of nonrandomized controlled trials that compared ECT with antidepressants drugs. The review revealed a significant superiority of ECT in all comparisons: ECT versus simulated ECT, ECT versus placebo, ECT versus antidepressants in general, ECT versus TCAs and ECT versus MAOIs. The nonrandomized controlled trials also revealed a significant statistical difference in favor of ECT when confronted with antidepressants drugs. Data analyzed suggest that ECT is a valid therapeutic tool for treatment of depression, including severe and resistant forms.
              Article 0 comments Cited 110 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Title: The British Journal of Psychiatry
                Abbreviated Title: Br J Psychiatry
                Publisher: Royal College of Psychiatrists
                ISSN (Print): 0007-1250
                ISSN (Electronic): 1472-1465
                Publication date Created: January 2018
                Publication date (Electronic): January 04 2018
                Publication date (Print): January 2018
                Volume: 212
                Issue: 1
                Pages: 19-26
                Article
                DOI: 10.1192/bjp.2017.11
                PubMed ID: 29433612
                SO-VID: 9945e38a-25c8-40b7-b0be-890da9f97fc2
                Copyright © © 2018
                License:

                https://www.cambridge.org/core/terms

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