Electroconvulsive therapy and structural neuroplasticity in neocortical, limbic and paralimbic cortex

Abstract

Electroconvulsive therapy (ECT) is a highly effective and rapidly acting treatment for severe depression. To understand the biological bases of therapeutic response, we examined variations in cortical thickness from magnetic resonance imaging (MRI) data in 29 patients scanned at three time points during an ECT treatment index series and in 29 controls at two time points. Changes in thickness across time and with symptom improvement were evaluated at high spatial resolution across the cortex and within discrete cortical regions of interest. Patients showed increased thickness over the course of ECT in the bilateral anterior cingulate cortex (ACC), inferior and superior temporal, parahippocampal, entorhinal and fusiform cortex and in distributed prefrontal areas. No changes across time occurred in controls. In temporal and fusiform regions showing significant ECT effects, thickness differed between patients and controls at baseline and change in thickness related to therapeutic response in patients. In the ACC, these relationships occurred in treatment responders only, and thickness measured soon after treatment initiation predicted the overall ECT response. ECT leads to widespread neuroplasticity in neocortical, limbic and paralimbic regions and changes relate to the extent of antidepressant response. Variations in ACC thickness, which discriminate treatment responders and predict response early in the course of ECT, may represent a biomarker of overall clinical outcome. Because post-mortem studies show focal reductions in glial density and neuronal size in patients with severe depression, ECT-related increases in thickness may be attributable to neuroplastic processes affecting the size and/or density of neurons and glia and their connections.

Short- and Long-term Cognitive Outcomes in Patients With Major Depression Treated With Electroconvulsive Therapy

“…However, several of these neuroplastic changes do not significantly relate to changes of clinical response. Specifically, in our prior studies, changes in hippocampal and ACC morphometry and functional connectivity between the dorsal ACC, mediodorsal thalamus, hippocampus, right anterior temporal, medial parietal, and posterior cingulate cortex show moderate relationships with ECT symptom improvements (51, 52, 54). It is thus plausible that changes in particular structural and functional networks may relate to changes in cognitive function occurring with ECT that are at least partially independent of changes in network activity relating to clinical outcome.…”

“…Other studies have reported ECT-induced normalizing effects in the structure and function of the brain. For example, in an overlapping sample, we have reported ECT-induced neuroplasticity in the hippocampus and amygdala (51), and increased cortical thickness of the bilateral anterior cingulate cortex (ACC), inferior and superior temporal, parahippocampal, entorhinal and fusiform cortex and in distributed prefrontal areas over the course of ECT (52). We have also shown significant increases of fractional anisotropy (FA) indicating improved structural connectivity in dorsal fronto-limbic circuits (53).…”

Pretreatment and early-treatment cortical thickness is associated with SSRI treatment response in major depressive disorder

“…EMBARC provides a unique opportunity to examine pretreatment and short-term alterations in brain structure occurring within the first week of SSRI and placebo treatment. Cortical thickness alterations in the 1-week interval used in this study have been shown to be detectable via 3T structural MRI, for example, in learning new tasks [42] and following electroconvulsive shock therapy [43]. EMBARC's double-blind, randomized, placebocontrolled structure provides a basis for understanding whether potential structural treatment response markers are specific to the SSRI, sertraline.…”

Neural correlates of reduced depressive symptoms following cognitive training for chronic traumatic brain injury

“…Reduced depressive symptom severity after cognitive training for TBI was related to increased cortical thickness over time only within the TBI‐plus‐depressive symptoms group (Figure ). The depression literature has reported increases in cortical thickness following treatment for depression (van Eijndhoven et al, ; Phillips, Batten, Tremblay, Aldosary, & Blier, ; Pirnia et al, ). Our study extends this line of research by demonstrating intervention‐induced neuroplasticity in TBI with comorbid depressive symptoms.…”