Electroconvulsive therapy is associated with a decrease in anhedonia and axial diffusivity in the medial forebrain
Ana Maria Rivas-Grajales1, Palig Mouradian2, George Papadimitriou2
1Division of Neuropsychiatry and Neuromodulation, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, USA; Department of Psychiatry, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA.
Background:
Electroconvulsive therapy (ECT) is the most effective treatment for major depressive disorder (MDD). This study used diffusion-weighted imaging (DWI) to evaluate the effects of ECT in the medial forebrain bundle (MFB), a prominent fiber pathway of the mesocorticolimbic system, and its relationship to the therapeutic effects in syndromic depression severity and dimensional positive valence symptoms (i.e., anhedonia).
Methods:
DWI data were acquired in 11 patients with MDD who underwent treatment with right unilateral (RUL)-ECT. Depression severity was assessed with the Quick Inventory of Depressive Symptoms (QIDS) and anhedonia with the Snaith Hamilton Pleasure Scale (SHAPS). The MFB was extracted using multi-tensor tractography. We compared fractional anisotropy (FA), radial diffusivity (RD), axial diffusivity (AD), and trace indices before and after RUL-ECT. We also evaluated the associations between changes in DWI measures and clinical response.
Results:
Analysis revealed that RUL-ECT led to a significant decrease in AD in the right MFB (t = 2.81, P = 0.018). We observed a significant association between greater AD decrease and improvement in depression severity (r = 0.66, P = 0.02) and anhedonia levels (r = 0.69, P = 0.018).
Conclusion:
RUL-ECT is associated with right-lateralized white matter neuroplastic changes in the MFB: the structural effects of ECT follow the laterality of the electrode placement. MFB diffusion changes correlate with the syndromic response in depression severity and the dimensional improvement in anhedonia. Our results suggest that the therapeutic response after ECT is achieved through topographically specific modulation of pathological networks involved in mood regulation, particularly positive valence and reward pathways.
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