Abstract

Traumatic brain injury (TBI) has become a concern in sports, automobile accidents and combat operations. A better understanding of the mechanics leading to a TBI is required to cope with both the short-term life-threatening effects and long-term effects of TBIs, such as the development chronic traumatic encephalopathy (CTE). Kornguth et al. (1) proposed that an inflammatory and autoimmune process initiated by a water hammer effect at the bases of the sulci of the brain is a mechanism of TBI leading to CTE. A major objective of this study is to investigate whether the water hammer effect is present due to blunt impacts through the use of computational models. Frontal blunt impacts were simulated with 2D finite element models developed to capture the biofidelic geometry of a human head. The models utilized the Arbitrary Lagrangian Eulerian (ALE) method to model a layer of cerebrospinal fluid (CSF) as a deforming fluid allowing for CSF to move in and out of sulci. During the simulated impacts, CSF was not observed to be driven into the sulci during the transient response. However, elevated shear strain levels near the base of the sulci were exhibited. Further, increased shear strain was present when differentiation between white and gray matter was taken into account. Both of the results support clinical observations of (1).

Highlights

  • The marked increase in incidence of Traumatic Brain Injury (TBI) in athletes engaged in contact sports and Soldiers returning from deployment over the past two decades has led to extensive research regarding the mechanisms causing this injury and potential treatments for the condition [1,2,3,4,5,6,7,8]

  • Neuropathological studies on brain samples recovered from patients who died following diagnosis with severe TBI were found to have changes in the brain parenchyma that are designated as Chronic Traumatic Encephalopathy (CTE) [7, 11]

  • During rapid deceleration of the head associated with forceful impacts, the apices of the gyri are the sites of initial contact with the calvarium and these regions might be anticipated to be the major site of injury; this is not the case

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Summary

Introduction

The marked increase in incidence of Traumatic Brain Injury (TBI) in athletes engaged in contact sports and Soldiers returning from deployment over the past two decades has led to extensive research regarding the mechanisms causing this injury and potential treatments for the condition [1,2,3,4,5,6,7,8]. Inflammatory changes in the brain including activation of microglia, generation of antibodies to neuronal and glial proteins, increased permeability of the blood brain barrier and changes in the expression of interleukins and cytokines are associated with the clinical status of the subject [1, 9, 10]. These changes frequently occur ten or more years after injuries have occurred. We undertook a computational modeling study to investigate the load transmission to the brain under blunt impact conditions and understand the load amplification mechanism at the base of the sulcus as observed in Kornguth et al [1]

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