Stress Driven Physiological Damage After Traumatic Brain Injuries

Development of a mathematical tool to predict the biomechanical damage in the secondary insult phase of a traumatic brain injury constitutes an important step in its prevention and clinical treatment. Secondary injuries are initiated by an accumulation of excess intracellular calcium resulting in the biochemical degradation of essential cell components. This thesis develops a holistic phenomenological model to predict the intraneuronal calcium ion accumulation and its subsequent detrimental effects such as protein dysfunctions resulting in microtubule rupture. We validate our model by comparing our predictions with the available clinical and experimental observations in the literature.