WCCM-ECCOMAS 2020 congress

Accepted abstract for oral communication

Congress cancelled due to COVID19

Numerical assessment of intracranial pulsatility in a brain aging context

A. Vallet¹, Y. Davit¹ , E. Schmidt² and S. Lorthois¹

1 Institut de Mécanique des Fluides de Toulouse, CNRS, Toulouse, France. alexandra.vallet@imft.fr, yohan.davit@imft.fr & sylvie.lorthois@imft.fr
2 CHU de Toulouse, ToNIC UMR 1214, INSERM, Toulouse, France. schmidt.e@chu-toulouse.fr

Key Words: Blood pulsatility, Intracranial pressure, Network modelling, Brain aging

Recent papers suggest that vascular alterations play a key role in early stages of dementia, including Alzheimer’s Disease [1,2]. An important component of cerebral blood circulation is its pulsatility [3]. Abnormal intracranial pulsatility has been associated with several neuropathologies [4], cortical thinning in older adults [5] and frailty [6], a risk factor for neurodegenerative diseases. It seems therefore to contribute to pathological brain aging.


Unlike other organs, the brain is enclosed within the rigid skull. The increase in volume of the arterial system at each cardiac cycle thus leads to an increase in intracranial pressure (ICP) which exerts mechanical constraints on intracranial tissues (parenchyma, capillaries and veins) and on the compliant spinal canal. As a result, it is thought that high ICP pulsatility may damage capillaries and lead to neurodegeneration [3-5]. However, this causality is not obvious as the system is governed by mechanical coupling between all the above components and depends on many parameters, including the cranio-spinal tissues mechanical properties as well as the macro- and micro-vascular properties. The lack of in vivo data makes it difficult to identify the dominant parameters and coupling effects, which are needed to understand the mechanisms linking vascular alterations, increased ICP pulsatility and neurodegeneration.

To address this issue, we present a numerical model of pulse wave transmission in a vascular network enclosed in a fluid filled compliant compartment. The model is based on the linearized axisymmetric Navier-Stokes equations, a linear elastic law for vessel wall deformation and a 0D description of the extravascular pressure. It is discretized with a finite volume method. The model is applied to both an idealized vascular network and a 3D mouse intracortical microvascular network. The first one is used to perform a variance-based sensitivity analysis in order to identify the most influential parameters and coupling effects. The second one is used to show how specific vascular alterations at the arterial, capillary or venous level can lead to a pathological redistribution of the intracranial pulsations down to the microvasculature level. Finally, the relevance of the results in a clinical context is discussed.

REFERENCES
[1] Iturria-Medina et al., Early role of vascular dysregulation on late-onset Alzheimer/’s disease based on multifactorial data-driven analysis. Nat Commun, vol. 7, p. 11934, 2016.
[2] Hernández et al., Neutrophil adhesion in brain capillaries reduces cortical blood flow and impairs memory function in Alzheimer’s disease mouse models, Nat Neuro, vol. 22, n°3, p. 413, 2019.
[3] Wagshul et al., The pulsating brain: A review of experimental and clinical studies of intracranial pulsatility, Fluids and Barriers of the CNS, vol. 8, p. 5, 2011.
[4] Stone et al., The Mechanical Cause of Age-Related Dementia (Alzheimer’s Disease): The brain is destroyed by the pulse, Journal of Alzheimer’s Disease, vol. 44, no 2, p. 355-373, 2015.
[5] Wåhlin et al., Intracranial pulsatility is associated with regional brain volume in elderly individuals, Neurobiology of Aging, vol. 35, no 2, p. 365-372, 2014.
[6] Vallet et al., Biomechanical response of the CNS is associated with frailty in NPH-suspected patients, Journal of Neurology, in press, 2020.

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