Electroconvulsive therapy and structural neuroplasticity in neocortical, limbic and paralimbic cortex.
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.
Department of Neurology, Ahamason-Lovelace Brain Mapping Center, University of California Los Angeles, Los Angeles, CA, USA.
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Pirnia
Department of Neurology, Ahamason-Lovelace Brain Mapping Center, University of California Los Angeles, Los Angeles, CA, USA.
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Joshi
Department of Neurology, Ahamason-Lovelace Brain Mapping Center, University of California Los Angeles, Los Angeles, CA, USA.
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Leaver
Department of Neurology, Ahamason-Lovelace Brain Mapping Center, University of California Los Angeles, Los Angeles, CA, USA.
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Vasavada
Department of Neurology, Ahamason-Lovelace Brain Mapping Center, University of California Los Angeles, Los Angeles, CA, USA.
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Njau
Department of Neurology, Ahamason-Lovelace Brain Mapping Center, University of California Los Angeles, Los Angeles, CA, USA.|Department of Psychiatry and Biobehavioral Sciences, University of California Los Angeles, Los Angeles, CA, USA.
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Woods
Department of Psychiatry and Biobehavioral Sciences, University of California Los Angeles, Los Angeles, CA, USA.
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0000-0003-2895-4212
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Espinoza
Department of Neurology, Ahamason-Lovelace Brain Mapping Center, University of California Los Angeles, Los Angeles, CA, USA.|Department of Psychiatry and Biobehavioral Sciences, University of California Los Angeles, Los Angeles, CA, USA.
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Narr
D000328:Adult; D004292:Dominance, Cerebral / Q000502:physiology; D004565:Electroconvulsive Therapy; D018728:Entorhinal Cortex / Q000000981:diagnostic imaging / Q000473:pathology; D005260:Female; D006179:Gyrus Cinguli / Q000000981:diagnostic imaging / Q000473:pathology; D006801:Humans; D007090:Image Interpretation, Computer-Assisted; D008032:Limbic System / Q000000981:diagnostic imaging* / Q000473:pathology; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D019579:Neocortex / Q000000981:diagnostic imaging* / Q000473:pathology; D009473:Neuronal Plasticity / Q000502:physiology*; D020534:Parahippocampal Gyrus / Q000000981:diagnostic imaging / Q000473:pathology; D012016:Reference Values; D013702:Temporal Lobe / Q000000981:diagnostic imaging / Q000473:pathology; D016896:Treatment Outcome