Sulcal Cavitation in Linear Head Acceleration: Possible Correlation With Chronic Traumatic Encephalopathy

Traumatic Brain Injury (TBI) is a significant public health and financial concern that is affecting tens of thousands of people in the United States annually. There were over a million hospital visits related to TBI in 2017. Along with immediate and short-term morbidity from TBI, chronic traumatic encephalopathy (CTE) can have life-altering, chronic morbidity, yet the direct linkage of how head impacts lead to this pathology remains unknown. A possible clue is that chronic traumatic encephalopathy appears to initiate in the depths of the sulci. The purpose of this study was to isolate the injury mechanism/s associated with blunt force impact events. To this end, drop tower experiments were performed on a human head phantom. Our phantom was fabricated into a three-dimensional extruded ellipsoid geometry made out of Polyacrylamide gelatin that incorporated gyri-sulci interaction. The phantom was assembled into a polylactic acid 3D-printed skull, surrounded with deionized water, and enclosed between two optical windows. The phantom received repetitive low-force impacts on the order of magnitude of an average boxing punch. Intracranial pressure profiles were recorded in conjunction with high-speed imaging, 25 k frames-per-second. Cavitation was observed in all trials. Cavitation is the spontaneous formation of vapor bubbles in the liquid phase resulting from a pressure drop that reaches the vapor pressure of the liquid. The observed cavitation was predominately located in the contrecoup during negative pressure phases of local intracranial pressure. To further investigate the cavitation interaction with the brain tissue phantom, a 2D plane strain computational model was built to simulate the deformation of gyrated tissue as a result from the initiation of cavitation bubbles seen in the phantom experiments. These computational experiments demonstrated a focusing of strain at the depths of the sulci from bubble expansion. Our results add further evidence that mechanical interactions could contribute to the development of chronic traumatic encephalopathy and also that fluid cavitation may play a role in this interaction.