Following peripheral injury, neuronal mitochondria within the spinal cord dorsal horn display increased levels of reactive oxygen species (ROS). Elevated ROS, a marker for mitochondrial dysfunction, is sustained through the chronic phase of neuropathic pain; this indicates an unmet antioxidant need within the CNS that contributes to pain chronicity. Previously, the multiple sclerosis drug dimethyl fumarate (DMF) has been shown to alleviate chronic pain via stimulation of the transcription factor Nrf2, triggering a broad antioxidant response in the dorsal root ganglia. However, gaps remain regarding the specific mechanisms of action by which DMF provides analgesic relief in the central nervous system. In this project, we aim to delineate a connection between systemic DMF administration and rescue of mitochondrial ROS within the spinal cord dorsal horn, providing mechanistic insight into the role of mitochondrial health in pain chronicity following peripheral injury. We show that DMF treatment attenuates chronic pain behaviours in mice, alongside an increase in Nrf2 nuclear localization and shifts in the nuclear/cytosolic ratio of Nrf2 within spinal cord dorsal horn neurons.