Traumatic brain injury (TBI) results from a sudden bump or jolt of the head. It is a growing public health problem that is responsible for significant neurological impairment. TBI can result in several debilitating side effects, including motor dysfunction, cognitive deficits, behavioral changes, and persistent pain. It also causes changes at the cellular level that can affect brain function long-term. Tissue damage initiates a variety of secondary injury pathologies, such as excitotoxicity, neuroinflammation, and oxidative damage. While there are very few pharmacological treatment options for TBI, opioids are commonly used to treat post-injury pain. While opioids are powerful analgesics, their clinical utility is hindered by side effects such as tolerance, addiction, respiratory depression, motor dysfunction, and constipation. Also, opioids alone are responsible for causing many of the same cellular pathologies as TBI, specifically oxidative damage. An increase in reactive oxygen species can deplete neurons of important antioxidants and promote apoptosis. Recently, peroxynitrite (PN) has been implicated in both analgesic tolerance and TBI-related damage. By stimulating neuroinflammation and apoptosis, PN significantly impairs neurological function following both TBI and chronic opioid administration. Therefore, this thesis explores the interaction between opioids and brain injury. It was hypothesized that animals treated with morphine after TBI or sham procedure will exhibit greater motor dysfunction and oxidative damage than those treated with a vehicle solution. While the results of this study are inconclusive, they provide a platform for further research on the subject.