Abstract

Traumatic spinal cord injury (SCI) is a devastating neurologic entity characterized by a primary insult followed by a secondary pathologic cascade that propagates further injury. Hypothermia has an established clinical role in preventing SCI after cardiac arrest and thoracoabdominal aortic aneurysm repair, yet its emergence as a potential neuroprotectant after spinal cord trauma remains experimental. There are currently no pharmacologic interventions available to prevent secondary mechanisms of injury after spinal cord trauma. Systematic review of literature. Experimental studies demonstrated that hypothermia diminishes secondary pathomechanisms, such as ischemia, oxidative stress, apoptosis, inflammation, and edema. Early onset and longer durations of hypothermia as well as concomitant steroids or neural stem cell engraftment combined with hypothermia appear to improve functional and histologic outcomes in animal models of spinal cord trauma. Recent clinical studies provide evidence that localized and systemic hypothermia may be applied safely and efficaciously in patients with severe acute SCI. Randomized clinical trials are needed to better evaluate optimal cooling parameters and the effectiveness of hypothermia after traumatic SCI. Although variability exists in the literature, therapeutic hypothermia most likely confers neuroprotection after spinal cord trauma by diminishing the destructive secondary cascade. The available clinical data suggest that regional and systemic hypothermia is a relatively safe and feasible initial treatment modality for patients with acute SCI when combined with surgical decompression/stabilization with or without steroids. However, establishing a clinical role for therapeutic hypothermia after spinal cord trauma will invariably depend on future well-designed, multicentered, randomized, controlled clinical trial data.

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