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Pathological Neural Attractor Dynamics in Slowly Growing Gliomas Supports an Optimal Time Frame for White Matter Plasticity

机译:胶质瘤生长缓慢的病理神经吸引因子动力学为白色物质可塑性提供了最佳时限

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摘要

Neurological function in patients with slowly growing brain tumors can be preserved even after extensive tumor resection. However, the global process of cortical reshaping and cerebral redistribution cannot be understood without taking into account the white matter tracts. The aim of this study was to predict the functional consequences of tumor-induced white matter damage by computer simulation. A computational model was proposed, incorporating two cortical patches and the white matter connections of the uncinate fasciculus. Tumor-induced structural changes were modeled such that different aspects of the connectivity were altered, mimicking the biological heterogeneity of gliomas. The network performance was quantified by comparing memory pattern recall and the plastic compensatory capacity of the network was analyzed. The model predicts an optimal level of synaptic conductance boost that compensates for tumor-induced connectivity loss. Tumor density appears to change the optimal plasticity regime, but tumor size does not. Compensatory conductance values that are too high lead to performance loss in the network and eventually to epileptic activity. Tumors of different configurations show differences in memory recall performance with slightly lower plasticity values for dense tumors compared to more diffuse tumors. Simulation results also suggest an optimal noise level that is capable of increasing the recall performance in tumor-induced white matter damage. In conclusion, the model presented here is able to capture the influence of different tumor-related parameters on memory pattern recall decline and provides a new way to study the functional consequences of white matter invasion by slowly growing brain tumors.
机译:即使进行广泛的肿瘤切除,脑肿瘤生长缓慢的患者的神经功能仍可以保留。但是,如果不考虑白质区域,就无法理解整个皮质重塑和大脑再分布的过程。这项研究的目的是通过计算机模拟预测肿瘤引起的白质损伤的功能后果。提出了一个计算模型,该模型结合了两个皮质斑块和松状束的白质连接。对肿瘤引起的结构变化进行建模,以便改变连接的不同方面,从而模仿神经胶质瘤的生物学异质性。通过比较记忆模式调用来量化网络性能,并分析了网络的塑性补偿能力。该模型预测突触传导增强的最佳水平,以补偿肿瘤引起的连接性丧失。肿瘤密度似乎改变了最佳可塑性方案,但肿瘤大小并未改变。补偿电导值太高会导致网络性能下降,并最终导致癫痫活动。不同形态的肿瘤表现出记忆回忆性能的差异,与较弥散性肿瘤相比,致密性肿瘤的可塑性值略低。仿真结果还提出了一种最佳噪声水平,该噪声水平能够提高肿瘤引起的白质损害的召回性能。总之,这里介绍的模型能够捕获不同的肿瘤相关参数对记忆模式回忆下降的影响,并为研究缓慢生长的脑瘤侵袭白质的功能后果提供了新的途径。

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