Blast traumatic brain injury (bTBI) is a leading cause of injury in the armed forces. Diffuse axonal injury, the hallmark feature of blunt TBI, has been investigated in direct mechanical loading conditions. However, recent evidence suggests inertial cavitation as a possible bTBI mechanism. Cavitation occurs via a low-pressure region caused by pressure waves, and is strongly dependent on local geometric and mechanical properties. The structural damage features as the result of cavitation-particularly at the cellular level-are incompletely understood. Microcavitation is induced via single, high-energy laser pulses, wherein single bubbles are generated within the focal plane of the sample, recorded at high-speed and analyzed with custom image processing algorithms. Initial work characterized distinct strain regimes where different modalities of cellular injury dominated, including complete cellular fragmentation, severe somatic and projection fragmentation, limited somatic damage with severe projection fragmentation, and limited projection damage. Preliminary actin fragmentation results indicated the presence of severe cytoskeletal disruptions up to the fragmentation radius dictated by cavitation bubble dynamics. The focus of this study is the examination of cytoskeletal disruption, including microtubule disruption and actin fragmentation. In addition, cellular viability and cellular apoptotic pathway studies are examined within the context of the larger pathology of bTBI.