Approximately 17,000 people sustain a spinal cord injury (SCI) in the U.S. each year, and over a quarter million Americans currently live with paralysis due to SCI. Injury severity and functional deficits due to SCI correlate with the extent of fluid accumulation (i.e., edema) occurring immediately after injury. Previous studies showed fluid pressure around the injured spinal cord (supraspinal) remains elevated for at least three days and contributes to a phase of tissue damage known as secondary injury. While neural cells will more directly interface with fluid within the spinal cord (interstitial), it is currently unknown how SCI affects interstitial fluid pressure and if interstitial forces also contribute to secondary injury. In this project, I will use a combination of in silico and in vivo models to address these questions. Understanding the contributions of fluid forces and flows after SCI may enable strategies to limit tissue damage and functional deficits after SCI.