Abstract: Traumatic spinal cord injury (SCI) is a pathological condition that impairs both sensorimotor and cognitive functions. While research has long focused on understanding the pathophysiology of SCI and developing treatments, only a few studies have investigated the cellular and molecular consequences that occur in the brain after trauma. From the earliest stages, the injury triggers microglial activation, increased neuronal death, and reduced hippocampal neurogenesis in the dentate gyrus, which in turn leads to cognitive impairments such as deficits in working memory, attention, learning capacity, and the detection and evaluation of stimuli (Li et al., 2020). These effects are a direct consequence of secondary damage following SCI and the onset of neuroinflammation, which can persist chronically.