Editorial

Abstract

The role and timing of decompression for acute spinal cord injury (SCI) remain an area of controversy. 3 Based on compelling preclinical data in relevant animal models and key clinicopathological studies, it is now generally well accepted that SCI involves a direct primary injury caused by a complex array of mechanical forces followed by a series of vascular and biomolecular processes that culminate in a secondary injury. 7 Ischemia is a key trigger that initiates the secondary injury cascade that includes derangements in cationic homeostasis, oxidative cell injury, glutamatergic excitotoxicity, inflammation, and apoptosis. Many clinicians and sci entists have long postulated that continued compression of the injured spinal cord due to bone, disc, or epidural blot clot could exacerbate ischemia and the secondary injury cascade. With this background, the Spine Trauma Study Group has been conducting a multicenter, prospective study (the Surgical Trial in Acute Spinal Cord Injury Study [STASCIS]) to evaluate the role and timing of decompression in patients with an acute cervical spinal cord injury. 5