A MATHEMATICAL INVESTIGATION OF THE ROLE OF INTRACRANIAL PRESSURE PULSATIONS AND SMALL GRADIENTS IN THE PATHOGENESIS OF HYDROCEPHALUS.

Kathleen P Wilkie, Corina S Drapaca, Sivabal Sivaloganathan
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Abstract

Cerebrospinal fluid (CSF) pulsations have been proposed as a possible causative mechanism for the ventricular enlargement that characterizes the neurological condition known as hydrocephalus. This paper summarizes recent work by the authors to anaylze the effect of CSF pulsations on brain tissue to determine if they are mechanically capable of enlarging the cerebral ventricles. First a poroelastic model is presented to analyze the interactions that occur between the fluid and porous solid constituents of brain tissue due to CSF pulsations. A viscoelastic model is then presented to analyze the effects of the fluid pulsations on the solid brain tissue. The combined results indicate that CSF pulsations in a healthy brain are incapable of causing tissue damage and thus the ventricular enlargement observed in hydrocephalus. Therefore they cannot be the primary cause of this condition. Finally, a hyper-viscoelastic model is presented and used to demonstrate that small long-term transmantle pressure gradients may be a possible cause of communicating hydrocephalus in infants.

颅内压力搏动和小梯度在脑积水发病机制中的作用的数学研究。
脑脊液(CSF)搏动被认为是脑室扩大的可能致病机制,而脑室扩大正是脑积水这种神经系统疾病的特征。本文总结了作者最近的工作,即分析 CSF 搏动对脑组织的影响,以确定 CSF 搏动是否能以机械方式使脑室扩大。首先介绍了一个孔弹性模型,用于分析 CSF 脉动引起的脑组织流体和多孔固体成分之间的相互作用。然后提出粘弹性模型,分析流体脉动对固体脑组织的影响。综合结果表明,健康大脑中的 CSF 脉动不会造成组织损伤,因此也不会导致脑积水中观察到的脑室扩大。因此,它们不可能是导致脑积水的主要原因。最后,我们提出了一个超弹性模型,并利用该模型证明,长期小的跨幔压力梯度可能是导致婴儿交流性脑积水的一个原因。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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