Abstract

BackgroundVolume increases of the hippocampus after electroconvulsive therapy (ECT) are a robust finding, pointing into the direction of neurogenesis. However, such volumetric increases could also be explained by edema and/or neuroplastic changes (such as angiogenesis). ObjectivesIf edema explains the volume increase of the hippocampus we hypothesize it would lead to increased mean diffusivity (MD). If neuroplastic would explain the volume increase, it would lead to decreased MD. To investigate angiogenesis as explanation we studied the perfusion fraction f and the pseudodiffusion component D∗ obtained from intravoxel incoherent motion (IVIM) data, and relative perfusion changes obtained from arterial spin labelling (ASL) data. MethodsUsing ultra-high field (7 tesla) MRI we acquired IVIM and ASL data. We compared MD, f, D∗ and ASL values for both hippocampi in 21 patients (before and after 10 ECT sessions) and 8 healthy controls (without ECT) in a linear mixed model adjusting for age and gender. ResultsWe found a significant decrease in MD (which was absent in the healthy controls) in the left and right hippocampus (t = -3.98, p < 0.001). In addition, a decrease in f (t = -4.61, p < 0.001, but not in controls) and no differences in D∗ or ASL perfusion values (both p > 0.05) were found. ConclusionsThe decrease in MD in perfusion fraction f suggest that formation of edema nor angiogenesis are responsible for the ECT-induced volume increases in the hippocampus. Also, it supports the hypothesis that hippocampal volume increases might be due to neuroplastic changes.

Highlights

  • Originated in the 1930s, electroconvulsive therapy (ECT) is the most effective treatment for severe major depression [1e4], and is still widely used today to treat refractory depressive disorders

  • In a previous study we used ultra-high field (7 T) magnetic resonance imaging (MRI) to measure changes in volume of the hippocampal subfields after ECT and reported a significant increase in volume exclusively for the DG [8]. To investigate whether this observed increase of DG volume could be explained by either angiogenesis or edema we investigate the hippocampus using diffusion weighted imaging (DWI; we acquired intravoxel incoherent motion (IVIM) data) and arterial spin labelling (ASL) in the same patient group receiving ECT

  • Using high field magnetic resonance imaging we investigated the effect of ECT on parameters of diffusivity and perfusion in the hippocampus

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Summary

Introduction

Originated in the 1930s, electroconvulsive therapy (ECT) is the most effective treatment for severe major depression [1e4], and is still widely used today to treat refractory depressive disorders. Research over the past decades focused on elucidating the mechanism by which ECT exerts its beneficial effects These efforts, benefitting from technological advancements of studying the brain in vivo and drawing from preclinical studies, yielded several important insights [5,6]. Volume increases of the hippocampus after electroconvulsive therapy (ECT) are a robust finding, pointing into the direction of neurogenesis. Such volumetric increases could be explained by edema and/or neuroplastic changes (such as angiogenesis). Conclusions: The decrease in MD in perfusion fraction f suggest that formation of edema nor angiogenesis are responsible for the ECT-induced volume increases in the hippocampus.

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