Traumatic spinal cord injury (SCI) has severe consequences for patients' physical, social, and vocational well-being. The demographic of SCI is shifting, with an increasing number of older individuals affected. Pathologically, the initial mechanical trauma (primary injury) damages neurons and glia, initiating a secondary injury cascade that leads to progressive cell death and spinal cord damage. Over time, the lesion remodels into cystic cavities and a glial scar, which inhibit regeneration. Animal models and behavioral tests are used to study SCI and develop preclinical and translational strategies. Diagnosis requires a thorough patient history, neurological examination, and imaging. Following diagnosis, interventions such as hemodynamic monitoring, surgical decompression, and methylprednisolone administration are applied. Managing complications like bowel and bladder dysfunction, pressure sores, and infections is crucial. SCI is defined as damage to the spinal cord that causes functional changes. It has traumatic and non-traumatic causes. Traumatic SCI results from external physical impact, while non-traumatic SCI results from diseases like tumors or degenerative disc disease. In traumatic SCI, the primary injury damages cells and initiates a secondary injury cascade, leading to neuronal and glial death, ischemia, and inflammation. This is followed by changes in spinal cord organization, including glial scar formation and cystic cavities. These structures, along with poor remyelination and axonal regrowth, limit spinal cord recovery. SCI has devastating physical, social, and vocational consequences, with patients experiencing loss of independence and increased mortality. The direct costs of SCI care are high, emphasizing the importance of prevention. Over the past three decades, numerous neuroprotective and neuroregenerative therapies have been translated into clinical trials. However, further progress requires better understanding of the pathophysiological cascade, limitations in translating animal model data, and combinatorial treatments. This Primer provides a foundation on SCI for new researchers, covering epidemiology, pathophysiology, and patient presentation. It discusses important therapeutic strategies, including medical, surgical, and cell-based treatments. The incidence of SCI varies globally, with higher rates in North America than in Australia or western Europe. Traumatic SCI is more common in males, with a bimodal age distribution. Traffic accidents are the primary cause of traumatic SCI in North America, followed by falls and sports-related injuries. High-energy impacts are more common in younger individuals, while low-energy impacts occur more in those over 60. The acute phase of SCI involves mechanical disruption, neuronal and oligodendrocyte injury, and vascular disruption, leading to a secondary injury cascade. Subacute and intermediate-chronic phases involve ischaemia, excitotoxicity, and inflammatory responses, contributing to further damage. The glial scar and cystic cavities inhibit regeneration, while the adult CNS myelin limits neurite regrowth. Remyelination is hindered by inflammatory responses and glial scar components. Endogenous repair mechanisms exist, butTraumatic spinal cord injury (SCI) has severe consequences for patients' physical, social, and vocational well-being. The demographic of SCI is shifting, with an increasing number of older individuals affected. Pathologically, the initial mechanical trauma (primary injury) damages neurons and glia, initiating a secondary injury cascade that leads to progressive cell death and spinal cord damage. Over time, the lesion remodels into cystic cavities and a glial scar, which inhibit regeneration. Animal models and behavioral tests are used to study SCI and develop preclinical and translational strategies. Diagnosis requires a thorough patient history, neurological examination, and imaging. Following diagnosis, interventions such as hemodynamic monitoring, surgical decompression, and methylprednisolone administration are applied. Managing complications like bowel and bladder dysfunction, pressure sores, and infections is crucial. SCI is defined as damage to the spinal cord that causes functional changes. It has traumatic and non-traumatic causes. Traumatic SCI results from external physical impact, while non-traumatic SCI results from diseases like tumors or degenerative disc disease. In traumatic SCI, the primary injury damages cells and initiates a secondary injury cascade, leading to neuronal and glial death, ischemia, and inflammation. This is followed by changes in spinal cord organization, including glial scar formation and cystic cavities. These structures, along with poor remyelination and axonal regrowth, limit spinal cord recovery. SCI has devastating physical, social, and vocational consequences, with patients experiencing loss of independence and increased mortality. The direct costs of SCI care are high, emphasizing the importance of prevention. Over the past three decades, numerous neuroprotective and neuroregenerative therapies have been translated into clinical trials. However, further progress requires better understanding of the pathophysiological cascade, limitations in translating animal model data, and combinatorial treatments. This Primer provides a foundation on SCI for new researchers, covering epidemiology, pathophysiology, and patient presentation. It discusses important therapeutic strategies, including medical, surgical, and cell-based treatments. The incidence of SCI varies globally, with higher rates in North America than in Australia or western Europe. Traumatic SCI is more common in males, with a bimodal age distribution. Traffic accidents are the primary cause of traumatic SCI in North America, followed by falls and sports-related injuries. High-energy impacts are more common in younger individuals, while low-energy impacts occur more in those over 60. The acute phase of SCI involves mechanical disruption, neuronal and oligodendrocyte injury, and vascular disruption, leading to a secondary injury cascade. Subacute and intermediate-chronic phases involve ischaemia, excitotoxicity, and inflammatory responses, contributing to further damage. The glial scar and cystic cavities inhibit regeneration, while the adult CNS myelin limits neurite regrowth. Remyelination is hindered by inflammatory responses and glial scar components. Endogenous repair mechanisms exist, but