NEURAL REPAIR AFTER SPINAL CORD INJURY: CELLULAR MECHANISMS AND EMERGING REGENERATIVE THERAPIES

Abstract

Spinal cord injury (SCI) initiates a biphasic process of primary mechanical damage followed by a secondary injury cascade involving ischemia, excitotoxicity, oxidative stress, and inflammation, which together determine the ultimate extent of neurological deficit. Endogenous repair is severely limited by formation of an astroglial-fibrotic scar, myelin-associated growth inhibitors, and the intrinsically weak regenerative capacity of adult central axons. Nevertheless, surviving spinal circuits below the level of injury retain a degree of activity-dependent plasticity that can be harnessed through locomotor training, epidural electrical stimulation, and functional electrical stimulation. Biological strategies targeting the glial scar, myelin inhibitors, and cell replacement are under active investigation, while brain-computer interfaces and neuroprosthetic devices offer alternative routes to restoring function. This review summarizes the cellular and molecular basis of spinal cord injury and repair, the influence of injury level and completeness on recovery potential, and current and emerging therapeutic strategies aimed at promoting functional neurological recovery.