Jorgensen A, Magnusson P, Hanson L G, Kirkegaard T, Benveniste H, Lee H, Svarer C, Mikkelsen J D, Fink-Jensen A, Knudsen G M, Paulson O B, Bolwig T G, Jorgensen M B
Psychiatric Centre Copenhagen (Rigshospitalet), Denmark.
Department of Neuroscience and Pharmacology, Laboratory of Neuropsychiatry, University of Copenhagen, Copenhagen, Denmark.
Acta Psychiatr Scand. 2016 Feb;133(2):154-164. doi: 10.1111/acps.12462. Epub 2015 Jul 3.
To investigate the role of hippocampal plasticity in the antidepressant effect of electroconvulsive therapy (ECT).
We used magnetic resonance (MR) imaging including diffusion tensor imaging (DTI) and proton MR spectroscopy ( H-MRS) to investigate hippocampal volume, diffusivity, and metabolite changes in 19 patients receiving ECT for severe depression. Other regions of interest included the amygdala, dorsolateral prefrontal cortex (DLPFC), orbitofrontal cortex, and hypothalamus. Patients received a 3T MR scan before ECT (TP1), 1 week (TP2), and 4 weeks (TP3) after ECT.
Hippocampal and amygdala volume increased significantly at TP2 and continued to be increased at TP3. DLPFC exhibited a transient volume reduction at TP2. DTI revealed a reduced anisotropy and diffusivity of the hippocampus at TP2. We found no significant post-ECT changes in brain metabolite concentrations, and we were unable to identify a spectral signature at ≈1.30 ppm previously suggested to reflect neurogenesis induced by ECT. None of the brain imaging measures correlated to the clinical response.
Our findings show that ECT causes a remodeling of brain structures involved in affective regulation, but due to their lack of correlation with the antidepressant effect, this remodeling does not appear to be directly underlying the antidepressant action of ECT.
探讨海马可塑性在电休克治疗(ECT)抗抑郁作用中的作用。
我们使用磁共振(MR)成像,包括扩散张量成像(DTI)和质子磁共振波谱(H-MRS),来研究19例接受ECT治疗重度抑郁症患者的海马体积、扩散率和代谢物变化。其他感兴趣的区域包括杏仁核、背外侧前额叶皮质(DLPFC)、眶额皮质和下丘脑。患者在ECT治疗前(TP1)、ECT治疗后1周(TP2)和4周(TP3)接受3T MR扫描。
海马和杏仁核体积在TP2时显著增加,并在TP3时持续增加。DLPFC在TP2时表现出短暂的体积减小。DTI显示在TP2时海马的各向异性和扩散率降低。我们发现ECT治疗后大脑代谢物浓度没有显著变化,并且我们无法识别先前认为反映ECT诱导神经发生的约1.30 ppm处的光谱特征。没有一项脑成像测量与临床反应相关。
我们的研究结果表明,ECT会导致参与情感调节的脑结构重塑,但由于它们与抗抑郁作用缺乏相关性,这种重塑似乎不是ECT抗抑郁作用的直接基础。