Mechanical loading of the ventricular wall as a spatial indicator for periventricular white matter degeneration.
Mechanical loading of the ventricular wall as a spatial indicator for periventricular white matter degeneration.
复制标题
心室壁的机械负荷作为脑室周围白质变性的空间指标。
DOI：
10.1016/j.jmbbm.2023.105921
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发表时间：
2023
影响因子：
3.9
通讯作者：
Weickenmeier,Johannes
中科院分区：
文献类型：
--
作者：
Visser,ValeryL;Caçoilo,Andreia;Rusinek,Henry;Weickenmeier,Johannes
在MRI扫描上，脑室周围和深部白色区域的进行性白色变性表现为白色高信号（WMH）。迄今为止，室周WMH通常与血管功能障碍有关。在这里，我们证明，心室膨胀导致脑萎缩和血液动力学脉动与每一次心跳导致的机械负荷状态的室周组织，显着影响心室壁。具体来说，我们提出了一个基于物理的建模方法，室管膜细胞参与室周WMH形成提供了一个合理的解释。建立在八个以前创建的二维有限元脑模型，我们引入新的mechanomarkers室管膜细胞负载和几何措施，侧脑室形状的特点。我们发现，我们的新的mechanomarkers，如最大室管膜细胞变形和最大曲率的心室壁，空间重叠与室周WMH的位置，是敏感的预测WMH的形成。我们还探讨了透明隔在减轻机械负荷的心室壁的作用，限制径向扩张的侧脑室在负荷。我们的模型一致表明，无论心室形状如何，室管膜细胞仅在心室角处被拉伸变薄。因此，我们认为脑室周围WMH的病因与过度拉伸的脑室壁恶化密切相关，导致CSF漏入脑室周围白色物质。随后的继发性损伤机制，包括血管变性，加剧病变形成并导致向深层白色物质区域进行性生长。
Progressive white matter degeneration in periventricular and deep white matter regions appears as white matter hyperintensities (WMH) on MRI scans. To date, periventricular WMHs are often associated with vascular dysfunction. Here, we demonstrate that ventricular inflation resulting from cerebral atrophy and hemodynamic pulsation with every heartbeat leads to a mechanical loading state of periventricular tissues that significantly affects the ventricular wall. Specifically, we present a physics-based modeling approach that provides a rationale for ependymal cell involvement in periventricular WMH formation. Building on eight previously created 2D finite element brain models, we introduce novel mechanomarkers for ependymal cell loading and geometric measures that characterize lateral ventricular shape. We show that our novel mechanomarkers, such as maximum ependymal cell deformations and maximum curvature of the ventricular wall, spatially overlap with periventricular WMH locations and are sensitive predictors for WMH formation. We also explore the role of the septum pellucidum in mitigating mechanical loading of the ventricular wall by constraining the radial expansion of the lateral ventricles during loading. Our models consistently show that ependymal cells are stretched thin only in the horns of the ventricles irrespective of ventricular shape. We therefore pose that periventricular WMH etiology is strongly linked to the deterioration of the over-stretched ventricular wall resulting in CSF leakage into periventricular white matter. Subsequent secondary damage mechanisms, including vascular degeneration, exacerbate lesion formation and lead to progressive growth into deep white matter regions.