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Vasogenic edema versus neuroplasticity as neural correlates of hippocampal volume increase following electroconvulsive therapy
Brain Stimulation ( IF 7.7 ) Pub Date : 2020-07-01 , DOI: 10.1016/j.brs.2020.04.017
Jasper O Nuninga 1 , René C W Mandl 2 , Martijn Froeling 3 , Jeroen C W Siero 4 , Metten Somers 2 , Marco P Boks 2 , Wendy Nieuwdorp 2 , Sophie Heringa 2 , Iris E C Sommer 5
Affiliation  

Abstract Background Volume increases of the hippocampus after electroconvulsive therapy (ECT) are a robust finding, pointing into the direction of neurogenesis. However, such volumetric increases could also be explained by edema and/or neuroplastic changes (such as angiogenesis). Objectives If edema explains the volume increase of the hippocampus we hypothesize it would lead to increased mean diffusivity (MD). If neuroplastic would explain the volume increase, it would lead to decreased MD. To investigate angiogenesis as explanation we studied the perfusion fraction f and the pseudodiffusion component D∗ obtained from intravoxel incoherent motion (IVIM) data, and relative perfusion changes obtained from arterial spin labelling (ASL) data. Methods Using ultra-high field (7 tesla) MRI we acquired IVIM and ASL data. We compared MD, f, D∗ and ASL values for both hippocampi in 21 patients (before and after 10 ECT sessions) and 8 healthy controls (without ECT) in a linear mixed model adjusting for age and gender. Results We found a significant decrease in MD (which was absent in the healthy controls) in the left and right hippocampus (t = -3.98, p 0.05) were found. Conclusions The decrease in MD in perfusion fraction f suggest that formation of edema nor angiogenesis are responsible for the ECT-induced volume increases in the hippocampus. Also, it supports the hypothesis that hippocampal volume increases might be due to neuroplastic changes.

中文翻译:

血管源性水肿与神经可塑性,因为电休克治疗后海马体积增加的神经相关性

摘要 背景 电休克疗法 (ECT) 后海马体的体积增加是一个强有力的发现,指向神经发生的方向。然而,这种体积增加也可以用水肿和/或神经可塑性变化(如血管生成)来解释。目标如果水肿解释了海马体积增加,我们假设它会导致平均扩散率 (MD) 增加。如果神经可塑性能解释体积增加,它将导致 MD 降低。为了研究血管生成作为解释,我们研究了从体素内非相干运动 (IVIM) 数据获得的灌注分数 f 和假扩散分量 D*,以及从动脉自旋标记 (ASL) 数据获得的相对灌注变化。方法使用超高场(7 特斯拉)MRI,我们获得了 IVIM 和 ASL 数据。我们比较了 MD、f、在调整年龄和性别的线性混合模型中,21 名患者(10 次 ECT 治疗前后)和 8 名健康对照(无 ECT)的海马 D* 和 ASL 值。结果 我们发现左右海马体的 MD 显着降低(健康对照中不存在)(t = -3.98,p = 0.05)。结论 灌注分数 f 中 MD 的降低表明水肿的形成和血管生成是 ECT 诱导的海马体积增加的原因。此外,它支持海马体积增加可能是由于神经可塑性变化的假设。结果 我们发现左右海马体的 MD 显着降低(健康对照中不存在)(t = -3.98,p = 0.05)。结论 灌注分数 f 中 MD 的降低表明水肿的形成和血管生成是 ECT 诱导的海马体积增加的原因。此外,它支持海马体积增加可能是由于神经可塑性变化的假设。结果 我们发现左右海马体的 MD 显着降低(健康对照中不存在)(t = -3.98,p = 0.05)。结论 灌注分数 f 中 MD 的降低表明水肿的形成和血管生成是 ECT 诱导的海马体积增加的原因。此外,它支持海马体积增加可能是由于神经可塑性变化的假设。
更新日期:2020-07-01
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