期刊
PSYCHOLOGICAL MEDICINE
卷 50, 期 5, 页码 849-856出版社
CAMBRIDGE UNIV PRESS
DOI: 10.1017/S0033291719000758
关键词
Biomarker; depression; DTI; ECT; FA; MD
资金
- German Research Foundation (DFG) [FOR2107 DA1151/5-1, DA1151/5-2, SFB-TRR58]
- Interdisciplinary Center for Clinical Research (IZKF) of the medical faculty of Munster [Dan3/012/17]
- IMF Munster [RE111604, RE111722, RE 22 17 07]
- Deanery of the Medical Faculty of the University of Munster
Background Electroconvulsive therapy (ECT) is a fast-acting intervention for major depressive disorder. Previous studies indicated neurotrophic effects following ECT that might contribute to changes in white matter brain structure. We investigated the influence of ECT in a non-randomized prospective study focusing on white matter changes over time. Methods Twenty-nine severely depressed patients receiving ECT in addition to inpatient treatment, 69 severely depressed patients with inpatient treatment (NON-ECT) and 52 healthy controls (HC) took part in a non-randomized prospective study. Participants were scanned twice, approximately 6 weeks apart, using diffusion tensor imaging, applying tract-based spatial statistics. Additional correlational analyses were conducted in the ECT subsample to investigate the effects of seizure duration and therapeutic response. Results Mean diffusivity (MD) increased after ECT in the right hemisphere, which was an ECT-group-specific effect. Seizure duration was associated with decreased fractional anisotropy (FA) following ECT. Longitudinal changes in ECT were not associated with therapy response. However, within the ECT group only, baseline FA was positively and MD negatively associated with post-ECT symptomatology. Conclusion Our data suggest that ECT changes white matter integrity, possibly reflecting increased permeability of the blood-brain barrier, resulting in disturbed communication of fibers. Further, baseline diffusion metrics were associated with therapy response. Coherent fiber structure could be a prerequisite for a generalized seizure and inhibitory brain signaling necessary to successfully inhibit increased seizure activity.
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