A mechanism for injury through cerebral arteriole inflation
An increase in arterial pressure within the cerebral vasculature appears to coincide with ischemia and dysfunction of the neurovascular unit in some cases of traumatic brain injury. In this study, we examine a new mechanism of brain tissue damage that results from excessive cerebral arteriole pressurization. We begin by considering the morphological and material properties of normotensive and hypertensive arterioles and present a computational model that captures the interaction of neighboring pressurized arterioles and the surrounding brain tissue. Assuming an axonal strain-induced injury criterion, we find that the injury depends on vessel spacing, proximity to an unconfined free surface, and the relative difference in stiffness between the arterioles and the surrounding tissue. We find that a steeper heterogeneity (stiffer vessels surrounded by softer brain tissue) causes larger axial strains to develop at some distance from the arteriole wall, within the brain parenchyma. For a more gradual heterogeneity (softer vessels), we observe more larger strain fields close to the arteriole walls. Both deformation patterns are comparable to damage seen in previous pathology studies on postmortem TBI patients. Finally, we use an analytical model to approximate the interplay between internal pressure, arteriole thickness, and the variation in mechanical properties of arterioles.
KeywordsCerebral vasculature Hypertension Traumatic brain injury TBI Finite element method
We would like to thank Dr. Ann Mae Dileonardi for help with proofreading the manuscript. The authors would also like to acknowledge Dr. Nitin Daphalapurkar, Dr. Jiwon Ryu, Dr. Vassilis Koliatsos, and Fatma Madouh for helpful conversations while writing this paper. This work was funded by the DoD SMART scholarship program and U.S. Army Research Lab under Cooperative Agreement No. W911NF-12-2-0022. The views and conclusions contained in this document are those of the authors and should not be interpreted as representing the official policies, either expressed or implied, of the Army Research Laboratory or the US Government. The US Government is authorized to reproduce and distribute reprints for Government purposes notwithstanding any copyright notation herein.
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Conflict of interest
The authors declare that they have no conflict of interest.
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