Abstract

Electroconvulsive therapy (ECT) is the most effective treatment for patients suffering from severe or treatment-resistant major depressive disorder (MDD). Unfortunately its underlying neurobiological mechanisms are still unclear. One line of evidence indicates that the seizures produced by ECT induce or stimulate neuroplasticity effects. Although these seizures also affect the cortex, the effect of ECT on cortical thickness is not investigated until now. We acquired structural magnetic resonance imaging data in 19 treatment-resistant MDD patients before and after a bilateral ECT course, and 16 healthy controls at 2 time points, and compared changes in cortical thickness between the groups. Our results reveal that ECT induces significant, bilateral increases in cortical thickness, including the temporal pole, inferior and middle temporal cortex and the insula. The pattern of increased cortical thickness was predominant in regions that are associated with seizure onset in ECT. Post hoc analyses showed that the increase in thickness of the insular cortex was larger in responders than in non-responders, which may point to a specific relationship of this region with treatment effects of ECT.

Highlights

  • Electroconvulsive therapy (ECT) is the most effective treatment for patients suffering from severe or treatment-resistant major depressive disorder (MDD),[1] achieving faster and higher response rates than pharmacotherapy,[2] the underlying neurobiological mechanisms remain poorly understood

  • There were no significant differences between MDD patients and healthy controls in age, sex distribution, level of education or handedness

  • We believe we show for the first time that electroconvulsive therapy (ECT) induces significant increases in cortical thickness in treatment

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Summary

Introduction

Electroconvulsive therapy (ECT) is the most effective treatment for patients suffering from severe or treatment-resistant major depressive disorder (MDD),[1] achieving faster and higher response rates than pharmacotherapy,[2] the underlying neurobiological mechanisms remain poorly understood. ECT-induced seizures engage both cortical and subcortical networks to varying degrees and result in increased cerebral blood blow in focal cortical areas.[6,7] In line with these broad hemodynamic effects of ECT on the brain, recent research indicates that next to effects on volume of hippocampus[8,9,10] or amygdala[11,12] ECT induces neuroplasticity effects in the cortex.[9,13] Up till there are no studies that have used cortical thickness analysis to investigate the effects of ECT treatment, which is a sensitive method to study longitudinal changes in the cortex.[14]

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