Abstract
Recent research suggests that neuroplastic and neuroinflammatory changes may account for the mode of action of electroconvulsive therapy (ECT), although extant data do not allow for a clear disambiguation between these two hypotheses. Multimodal neuroimaging approaches (for example, combining structural and metabolic information) may help in clarifying this issue. Here we aimed to assess longitudinal changes in (i) regional gray matter (GM) volumes and (ii) hippocampal metabolite concentrations throughout an acute course of bitemporal ECT, as well as (iii) to determine the association between imaging changes and clinical improvement. We assessed 12 patients with treatment-resistant depression (TRD) at four time points (pre-treatment, after the first ECT session, after the ninth ECT session and 15 days after ECT course completion) and 10 healthy participants at two time points, 5 weeks apart. Patients with TRD showed bilateral medial temporal lobe (MTL) and perigenual anterior cingulate cortex volume increases. Left MTL volume increase was associated with (i) a hippocampal N-acetylaspartate concentration decrease, (ii) a hippocampal Glutamate+Glutamine concentration increase and (iii) significant clinical improvement. The observed findings are, in part, compatible with both neuroplastic and neuroinflammatory changes induced by ECT. We postulate that such phenomena may be interrelated, therefore reconciling the neuroplasticity and neuroinflammatory hypotheses of ECT action.
Highlights
Electroconvulsive therapy (ECT) is a well-established alternative for treatment-resistant depression (TRD).[1]
Recent reports advocated that such electroconvulsive therapy (ECT)-induced structural changes could result from neurogenesis induction in neurogenic regions, the extension of volume increases to other hippocampal subfields and limbic regions[14] suggests that they are likely better understood as resulting from more general structural neuroplastic changes, which embrace different molecular mechanisms in addition to neurogenesis, such as synaptogenesis, gliogenesis or angiogenesis.[15]
The reduction in depression severity (HRSD score) between MRI1 and MRI4 assessments was significant according to a Wilcoxon signed-rank test (z = −3.062; P = 0.002)
Summary
Electroconvulsive therapy (ECT) is a well-established alternative for treatment-resistant depression (TRD).[1] its mechanism of action remains poorly understood. Recent studies have used magnetic resonance imaging (MRI) to explore the changes in brain structure putatively associated with ECT and have consistently reported volume increases in limbic regions such as the hippocampus, the amygdala or the anterior cingulate cortex (ACC).[2,3,4,5,6,7,8,9,10,11,12]. Induced structural changes might partially depend on neuroinflammatory mechanisms.[8,16] It has been shown that ECT may increase the permeability of the blood–brain barrier,[17] possibly leading to a local swelling of adjacent brain tissue (that is, vasogenic edema).[16]
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