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Regional brain volumes, diffusivity, and metabolite changes after electroconvulsive therapy for severe depression
Author(s) -
Jorgensen A.,
Magnusson P.,
Hanson L. G.,
Kirkegaard T.,
Benveniste H.,
Lee H.,
Svarer C.,
Mikkelsen J. D.,
FinkJensen A.,
Knudsen G. M.,
Paulson O. B.,
Bolwig T. G.,
Jorgensen M. B.
Publication year - 2016
Publication title -
acta psychiatrica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.849
H-Index - 146
eISSN - 1600-0447
pISSN - 0001-690X
DOI - 10.1111/acps.12462
Subject(s) - electroconvulsive therapy , fractional anisotropy , hippocampal formation , neuroscience , psychology , hippocampus , orbitofrontal cortex , dorsolateral prefrontal cortex , antidepressant , diffusion mri , major depressive disorder , magnetic resonance imaging , medicine , prefrontal cortex , amygdala , cognition , radiology
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 ( 1 H ‐ 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 3 T MR scan before ECT ( TP 1), 1 week ( TP 2), and 4 weeks ( TP 3) after ECT . Results Hippocampal and amygdala volume increased significantly at TP 2 and continued to be increased at TP 3. DLPFC exhibited a transient volume reduction at TP 2. DTI revealed a reduced anisotropy and diffusivity of the hippocampus at TP 2. 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 .