Regional brain volumes, diffusivity, and metabolite changes after electroconvulsive therapy for severe depression

Objective To investigate the role of hippocampal plasticity in the antidepressant effect of electroconvulsive therapy (ECT). Method We used magnetic resonance (MR) imaging including diffusion tensor imaging (DTI) and proton MR spectroscopy (1H‐MRS) to investigate hippocampal volume, diffusivity, and...

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Bibliographic Details
Published in:Acta psychiatrica Scandinavica 2016-02, Vol.133 (2), p.154-164
Main Authors: Jorgensen, A., Magnusson, P., Hanson, L. G., Kirkegaard, T., Benveniste, H., Lee, H., Svarer, C., Mikkelsen, J. D., Fink-Jensen, A., Knudsen, G. M., Paulson, O. B., Bolwig, T. G., Jorgensen, M. B.
Format: Article
Language:English
Subjects:
depression
diffusion tensor imaging
Electroconvulsive therapy
hippocampus
magnetic resonance imaging
magnetic resonance spectroscopy
Mental depression
Metabolites
Neuropsychology
Psychiatry
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Summary:Objective To investigate the role of hippocampal plasticity in the antidepressant effect of electroconvulsive therapy (ECT). Method We used magnetic resonance (MR) imaging including diffusion tensor imaging (DTI) and proton MR spectroscopy (1H‐MRS) to investigate hippocampal volume, diffusivity, and metabolite changes in 19 patients receiving ECT for severe depression. Other regions of interest included the amygdala, dorsolateral prefrontal cortex (DLPFC), orbitofrontal cortex, and hypothalamus. Patients received a 3T MR scan before ECT (TP1), 1 week (TP2), and 4 weeks (TP3) after ECT. Results Hippocampal and amygdala volume increased significantly at TP2 and continued to be increased at TP3. DLPFC exhibited a transient volume reduction at TP2. DTI revealed a reduced anisotropy and diffusivity of the hippocampus at TP2. We found no significant post‐ECT changes in brain metabolite concentrations, and we were unable to identify a spectral signature at ≈1.30 ppm previously suggested to reflect neurogenesis induced by ECT. None of the brain imaging measures correlated to the clinical response. Conclusion Our findings show that ECT causes a remodeling of brain structures involved in affective regulation, but due to their lack of correlation with the antidepressant effect, this remodeling does not appear to be directly underlying the antidepressant action of ECT.
ISSN:0001-690X
1600-0447
DOI:10.1111/acps.12462