Traumatic spinal cord injury (SCI) has devastating physical, social, and vocational consequences for patients, with an increasing proportion of older individuals being affected. The initial mechanical trauma (primary injury) initiates a secondary injury cascade, leading to progressive cell death and spinal cord damage over weeks. The lesion remodels into cystic cavitations and a glial scar, both of which inhibit regeneration. Animal models and behavioral tests have been developed to mimic these pathological processes, forming the basis for neuroprotective and neuroregenerative strategies. Diagnosis involves a thorough patient history, neurological examination, and radiographic imaging. Rapid interventions, including hemodynamic monitoring, early surgical decompression, blood pressure augmentation, and methylprednisolone administration, are crucial. Managing complications such as bowel and bladder dysfunction, pressure sores, and infections is essential. The incidence of SCI varies globally, with higher rates in North America due to higher rates of violent crime and self-harm. Traumatic SCI is more common in males and has a bimodal age distribution, with a growing peak in individuals over 50 years old. Traffic accidents and falls are the primary causes, while cervical SCI is associated with higher mortality rates. Acute injury phase involves mechanical disruption, cell permeabilization, ischaemia, and inflammation, leading to further damage. Subacute and chronic phases are marked by remyelination attempts, vascular reorganization, and ECM changes, but these efforts are often hindered by cystic cavities and glial scars. Endogenous repair mechanisms, such as neural precursor cell pools, can contribute to partial regeneration. Animal models, particularly rats, have been instrumental in understanding SCI pathophysiology and testing therapies. Diagnosis relies on clinical examination, imaging, and electrophysiological recordings, with the International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI) providing a standardized approach. Prognosis and functional outcomes depend on the severity and location of the injury, with neurological recovery typically observed within the first 6 months. Management emphasizes rapid diagnosis and neuroprotective interventions, with ongoing research focusing on overcoming barriers to regeneration.Traumatic spinal cord injury (SCI) has devastating physical, social, and vocational consequences for patients, with an increasing proportion of older individuals being affected. The initial mechanical trauma (primary injury) initiates a secondary injury cascade, leading to progressive cell death and spinal cord damage over weeks. The lesion remodels into cystic cavitations and a glial scar, both of which inhibit regeneration. Animal models and behavioral tests have been developed to mimic these pathological processes, forming the basis for neuroprotective and neuroregenerative strategies. Diagnosis involves a thorough patient history, neurological examination, and radiographic imaging. Rapid interventions, including hemodynamic monitoring, early surgical decompression, blood pressure augmentation, and methylprednisolone administration, are crucial. Managing complications such as bowel and bladder dysfunction, pressure sores, and infections is essential. The incidence of SCI varies globally, with higher rates in North America due to higher rates of violent crime and self-harm. Traumatic SCI is more common in males and has a bimodal age distribution, with a growing peak in individuals over 50 years old. Traffic accidents and falls are the primary causes, while cervical SCI is associated with higher mortality rates. Acute injury phase involves mechanical disruption, cell permeabilization, ischaemia, and inflammation, leading to further damage. Subacute and chronic phases are marked by remyelination attempts, vascular reorganization, and ECM changes, but these efforts are often hindered by cystic cavities and glial scars. Endogenous repair mechanisms, such as neural precursor cell pools, can contribute to partial regeneration. Animal models, particularly rats, have been instrumental in understanding SCI pathophysiology and testing therapies. Diagnosis relies on clinical examination, imaging, and electrophysiological recordings, with the International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI) providing a standardized approach. Prognosis and functional outcomes depend on the severity and location of the injury, with neurological recovery typically observed within the first 6 months. Management emphasizes rapid diagnosis and neuroprotective interventions, with ongoing research focusing on overcoming barriers to regeneration.