Traumatic Brain Injury (TBI) has become a marquee injury of this generation, prevalent in both military and civilian populations (Meaney 2014). Blunt impacts to the head are the known cause of approximately 1.7 million of TBI hospitalizations per year (Meaney 2014), and while mild TBI has the highest incidence (approximately 75% of TBIs) the injuries range from mild concussions to life threating severe bleeding within the brain (Meaney 2014).

Due to wide spread prominence, blunt impact TBI has garnered a wealth of academic research interest focusing on the full spectrum of the biological scale, from subcellular and cellular response, to global human body modeling. The foundational theory of current blunt impact TBI research is neurological tissue damage by simple shear strain caused by motion of the skull (Cullen 2016, Alshareef 2020). While this likely contributes to tissue damage, its global perspective does not provide a satisfactory solution to the focal symptomology of TBI etiology. This is most likely because there are less appreciated mechanisms of injury contributing to TBI such as shear shock formation or cerebrospinal fluid (CSF) cavitation.

The focus of this dissertation is to unpack the role of CSF cavitation in blunt impact TBI and contribute an important piece missing from the mechanistic understanding of TBI. This work develops an acoustic biomarker that indicates transient cavitation collapse, uses this biomarker to investigate cavitation mechanisms, observes cavitation in fresh, non-frozen, full body pig cadaver blunt impact testing, and provides clinical implications for transient cavitation through a reanalysis of live subhuman primate seminal data. It takes advantage of the large magnitude wideband acoustic emission of transient cavitation collapse, advanced acoustic sensor technology, and novel acoustic analysis methods to uncover a piece of the mechanistic mystery surrounding blunt impact TBI.

There are five major conclusions reached in this dissertation. 1:​ The blunt impact head kinematics that induce cavitation are not significantly influenced by neck strength or cervical muscle activation. 2:​ Broadband acoustic emissions can be used as an acoustic biomarker to detect the incidence of transient cavitation collapse through the skull. 3:​ Compliance of the vessel containing a cavitating medium significantly influences the levels at which cavitation occurs during a blunt impact. 4:​ Blunt impact CSF cavitation occurs in a fresh, non-frozen, uncompromised pig cadaver head at impact levels below catastrophic injury thresholds. 5:​ Brain contusions are a potential clinical implication of transient cavitation collapse.

Due to a lack of tools and technology, previous work on blunt impact cavitation was restricted to experimentation with limitations prohibiting the direct study of intracranial transient CSF cavitation. This innovative work provides direct observation of blunt impact CSF cavitation that benefits tools, injury risk functions, safety device design, and detection methodologies.