During the past several years, results of clinical trials have generated considerable optimism about the prospects for effective treatment of acute central nervous system (CNS) injuries. A multicenter trial demonstrated the effectiveness of methylprednisolone, as well as naloxone hydrochloride, in improving neurologic recovery after spinal cord injury.1 In ischemic stroke, early treatment with tissue plasminogen activator2 or treatment with low-molecular-weight heparin3 led to improved outcome for some patients. To date, however, no effective pharmacotherapy has been developed for head injury.
One of the more promising experimental strategies for treatment of acute CNS injury has been the use of antioxidants or free-radical scavengers. This approach is based on the concept that oxygen free radicals are generated in response to the insult, thereby overwhelming endogenous antioxidant or free radical-scavenging systems such as superoxide dismutase (SOD), catalase, glutathione, ascorbic acid, and α-tocopherol.4,5 Free radicals are believed to contribute to
Faden AI. Pharmacologic Treatment of Acute Traumatic Brain Injury. JAMA. 1996;276(7):569–570. doi:10.1001/jama.1996.03540070065034
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