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Title
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The basal ganglia : a central hub for the psychomotor effects of electroconvulsive therapy
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Author
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Abstract
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| Background: Electroconvulsive therapy (ECT) is the most effective biological treatment for depression. Aside the well-known therapeutic effect on mood symptoms, it has also a unique positive impact on psychomotor agitation and retardation, which are core symptoms of depression. The neurobiology behind these effects, however, remains unclear. The basal ganglia are proposed to be important regions in the pathogenesis of psychomotor symptoms in depression. Since ECT can trigger neuroplasticity in these subcortical nuclei, we speculate that ECT-induced volumetric changes of the basal ganglia will positively influence psychomotor symptoms. Methods: Psychomotor symptoms were analyzed in 17 patients with severe depression before and after an acute ECT course using a CORE assessment of the retardation, agitation, and non-interaction domains. The volumes of the caudate, putamen, pallidum, and accumbens regions were determined using magnetic resonance imaging one week before and after ECT. Results: Psychomotor functions had improved significantly after ECT and significant volume increases were found for the accumbens region, the putamen, and pallidum. The volume increase of the nucleus accumbens correlated with an improvement of psychomotor retardation, while the volume increase of the pallidum correlated negatively with an improvement of the agitation subscore. Conclusion: Our findings support the notion of an association between the impact of ECT on depression-related psychomotor symptoms and volume increases of the accumbens region and pallidum, pointing to the importance of the basal ganglia in the therapeutic effect of ECT on psychomotor functioning. |
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Language
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English
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Source (journal)
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Journal of affective disorders. - Amsterdam
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Publication
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Amsterdam
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2020
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ISSN
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0165-0327
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DOI
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10.1016/J.JAD.2020.01.033
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Volume/pages
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265
(2020)
, p. 239-246
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ISI
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000514822200032
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Pubmed ID
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32090747
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Full text (Publisher's DOI)
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Full text (publisher's version - intranet only)
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