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Objectives: To assemble an algorithm that will describe a “Signature” predictive of an individual’s vulnerability to persistent traumatic brain injury (TBI) Subjects and Methods: Studies of athletes and warriors who are subjected to repeated head impacts with rapid acceleration/deceleration forces are used to assist in the diagnosis and management of TBI-affected individuals. Data from multiple areas, including clinical, anatomical, magnetic resonance imaging, cognitive function, and biochemical analyses, are integrated to provide a Signature of persistent TBI. Results: Studies to date indicate that susceptibility to TBI results from an interaction between host genetic and structural vulnerability factors and force and torque of impact on the head and torso. The host factors include molecular markers affecting immune and inflammatory responses to stress/insult as well as anatomical features such as the degree of transcortical fiber projections and vascular malformations. The host response to forceful impact includes the release of intracellular neural proteins and nucleic acids into the cerebrospinal fluid and vascular compartment as well as mobilization of cytokines and macrophages into the central nervous system with subsequent activation of microglia and inflammatory responses including autoimmune processes. Maximum impact to the base of the sulci via a “water hammer effect” is consistent with the localization of microvascular and inflammatory responses in the affected brain region. Conclusions: An assessment of an individuals’ predisposition to persistent TBI with delayed cognitive deficits and behavioral changes requires an understanding of host vulnerability (genetic factors and brain structure) and external stressors (force and torque of impact as well as repetitive head injury and time interval between impacts). An algorithm that has utility in predicting vulnerability to TBI will include qualitative and quantitative measures of the host factors weighted against post impact markers of neural injury. Implementation of the resulting “Signature” of vulnerability at early stages of injury will help inform athletes and warriors, along with commanders and management, of the risk/benefit approaches that will markedly diminish health care costs to the nation and suffering to this population. This report attempts to define a strategy to create such an algorithm.

During the past decade, there has been an increasing interest in early diagnosis and treatment of traumatic brain injuries (TBI) that lead to chronic traumatic encephalopathy (CTE). The subjects involved range from soldiers exposed to concussive injuries from improvised explosive devices (IEDs) to a significant number of athletes involved in repetitive high force impacts. Although the forces from IEDs are much greater by a magnitude than those from contact sports, the higher frequency associated with contact sports allows for more controlled assessment of the mechanism of action. In our study, we report findings in university-level women soccer athletes followed over a period of four and a half years from accession to graduation. Parameters investigated included T1-, T2-, and susceptibility-weighted magnetic resonance images (SWI), IMPACT (Immediate Post-Concussion Assessment and Cognitive Testing), and C3 Logix behavioral and physiological assessment measures. The MRI Studies show several significant findings: first, a marked increase in the width of sulci in the frontal to occipital cortices; second, an appearance of subtle hemorrhagic changes at the base of the sulci; third was a sustained reduction in total brain volume in several soccer players at a developmental time when brain growth is generally seen. Although all of the athletes successfully completed their college degree and none exhibited long term clinical deficits at the time of graduation, the changes documented by MRI represent a clue to the pathological mechanism following an injury paradigm. The authors propose that our findings and those of prior publications support a mechanism of injury in CTE caused by an autoimmune process associated with the release of neural proteins from nerve cells at the base of the sulcus from a water hammer injury effect. As evidence accumulates to support this hypothesis, there are pharmacological treatment strategies that may be able to mitigate the development of long-term disability from TBI.

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).