Spinal cord injury (SCI) is a catastrophic condition resulting in significant sensory and motor neurological deficits. It imposes a substantial socioeconomic burden alongside severe physical impairment. SCI affects nearly all physiological systems in the body, significantly diminishing patient quality of life and, in severe cases, leading to death.1 Epidemiological data suggest that 40–50% of SCI cases are caused by traffic accidents. Young individuals are particularly vulnerable because of high-speed and high-impact activities such as diving, parachuting and mountain climbing, whereas falls are the predominant cause of SCI in older adults.2 Globally, an estimated 250 000–500 000 new SCI cases occur annually.3 The initial primary impact causes damage to the spinal cord, which is responsible not only for sensory or motor function loss but also initiating a secondary injury cascade that causes further destruction via the cascade of events such as inflammation, apoptosis, excitotoxicity, oxidative stress, mitochondrial dysfunction, compromised blood–spinal-cord barrier (BSCB) integrity and glial scar formation.[4], [5] However, the secondary injury cascade obstructs neuroregeneration and the restoration of neurological function.3 Injury severity and location determine the clinical outcomes.6

Despite extensive research into SCI pathophysiology, effective pharmacological and non-pharmacological treatments remain limited. No drug has been approved specifically for trauma-induced SCI.7 Early surgical decompression (within 24 h post-injury) is currently one of the most effective interventions.6 Whereas some treatments have reached clinical trials, their successful translation into clinical practice remains challenging. This review covers the pathophysiology of SCI, pharmacological and non-pharmacological strategies currently being researched, as well as various interventions that are currently at the clinical trial level or at the transient stage of the clinical trial.