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.
Highlights
The high rates of major depression, affecting an estimated 350 million people worldwide,[1] and the only moderate success rates of available antidepressant treatments underscore the importance of unraveling the biological bases of therapeutic response
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 Electroconvulsive therapy (ECT) treatment index series and in 29 controls at two time points
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
Summary
The high rates of major depression, affecting an estimated 350 million people worldwide,[1] and the only moderate success rates of available antidepressant treatments underscore the importance of unraveling the biological bases of therapeutic response. Whereas neurogenesis is observed in the hippocampus, gliogenesis and pronounced volumetric changes are found in additional areas including the amygdala and prefrontal cortex after ECS.[7,8,9,10,11,12,13] Recently, molecular markers of adult neurogenesis have been reported in frontal areas in days to weeks after ECS.[14] studies using pharmacological interventions induce similar treatment-related cell proliferation, these effects appear less pronounced in comparison with ECT.[14] Post-mortem studies further demonstrate that depressed patients have reduced glial cell density and neuronal size compared with healthy volunteers in prefrontal regions including the anterior cingulate cortex (ACC), and connected dorsolateral (DLPFC) and ventral (VPFC) prefrontal cortices.[15,16,17] Correspondingly, neuroimaging studies report an altered brain structure in depression, including reductions in the cortical gray matter;[18,19,20] alterations in structure of the ACC, DLPFC, VPFC and ventromedial prefrontal cortex are frequently linked with the disorder.[21,22,23] Taken together, these data support a neurotrophic model of depression and antidepressant response, suggesting that ECT may elicit structural plasticity within prefrontal and limbic regions.
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