Numerical modelling of multiple sclerosis: A tissue-scale model of brain lesions

Q3 Engineering Brain multiphysics Pub Date : 2024-08-08 DOI:10.1016/j.brain.2024.100097
H Hutchison , AC Szekely-Kohn , W Li , DET Shepherd , DM Espino
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Abstract

Multiple Sclerosis (MS) is an autoimmune condition leading to the degeneration of brain tissue, occurring when the immune system attacks the myelin sheath surrounding axons of white brain matter thereby disrupting brain signals. This study aimed to evaluate how MS lesions alter stress distribution through grey and white brain matter with lesions (active, chronic, and inactive). A linear viscoelastic model represents the tissue-scale dynamic deformation and time dependency of brain tissue. A Prony series expansion was used to model viscous effects including stress relaxation. An elastic modulus, within the viscoelastic model, was either reduced by 11 % for active lesions, or increased by 35 % increase for inactive lesions. These material properties were then implemented to model healthy tissue, active, chronically inflamed, and inactive lesions. Finite element analysis enabled stress evaluation in response to a peak cyclic displacement of 0.5 mm (1 % strain) with the healthy model acting as a control model. Chronic lesions had the largest effect on stress induced, in terms of high (171 Pa) and low stress (108 Pa). Inactive lesions induced an increase in stress of 11 Pa with areas of low stress (105 Pa). Active lesions caused the least deviation in peak induced stress (7 Pa). In conclusion, a hierarchy in stress induced across the lesion types has been found, from highest to lowest: chronic, inactive and active, with potential implications for lesion progression. In conclusion, MS lesions within brain tissue should model lesions, avoid assuming homogeneity during degeneration, and should distinguish between active and passive lesions.

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多发性硬化症的数值建模:脑损伤组织尺度模型
多发性硬化症(MS)是一种导致脑组织变性的自身免疫性疾病,当免疫系统攻击白色脑物质轴突周围的髓鞘时,就会破坏脑信号。本研究旨在评估多发性硬化症病变(活动性、慢性和非活动性)如何改变脑灰质和脑白质的应力分布。线性粘弹性模型表示了脑组织的组织尺度动态变形和时间依赖性。普罗尼序列扩展用于模拟粘性效应,包括应力松弛。在粘弹性模型中,活跃病变的弹性模量降低了 11%,不活跃病变的弹性模量增加了 35%。这些材料特性随后被应用于健康组织、活跃病变、慢性炎症病变和非活跃病变的建模。通过有限元分析,可以对 0.5 毫米(1% 应变)的峰值循环位移进行应力评估,健康模型作为对照模型。慢性病变对应力的影响最大,包括高应力(171 帕)和低应力(108 帕)。非活动性病变引起的应力增加了 11 帕,低应力区域为 105 帕。活性病变引起的峰值应力偏差最小(7 Pa)。总之,我们发现不同病变类型引起的应力从高到低:慢性病变、非活动性病变和活动性病变,这对病变的进展具有潜在的影响。总之,脑组织内的多发性硬化病变应建立病变模型,避免假定退化过程中的同质性,并应区分活动性和被动性病变。
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来源期刊
Brain multiphysics
Brain multiphysics Physics and Astronomy (General), Modelling and Simulation, Neuroscience (General), Biomedical Engineering
CiteScore
4.80
自引率
0.00%
发文量
0
审稿时长
68 days
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