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Methylprednisolone exacerbates axonal loss following optic nerve trauma in rats

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PURPOSE: This study investigates the clinical dogma that very high doses of methylprednisolone helpful in spinal cord injury are also helpful in optic nerve trauma. Methods: The right optic nerve of 29 male rats received a 5 second traumatic crush followed 30 minutes later by one of five intravenous treatments (methylprednisolone 30 mg/kg, 60 mg/kg, 90 mg/kg, 120 mg/kg, or saline). Treatment was continued for three additional administrations at 6 hour intervals. Untreated sham controls (n = 7) were also prepared. Six weeks after injury, animals were sacrificed, perfused and optic nerves systematically counted. RESULTS: Axon counts (means +/− s.e.m.) were as follows: Saline = 16,670 +/− 8,900 (n = 5); Methylprednisolone: 30 mg/kg = 8,098 +/− 4,741 (n = 5); 60 mg/kg = 6,925 +/− 6,517 (n = 4); 90 mg/kg = 2,663 +/− 2,653 (n = 4); 120 mg/kg = 6,149 +/− 3,487 (n = 6). Consequently, the data revealed that saline treated animals retained more axons than those that were administered methylprednisolone (p < 0.02). CONCLUSIONS: We conclude that methylprednisolone exacerbates axonal loss following crush injury in the rat optic nerve. Based on the results of this study, clinical studies of traumatic optic neuropathy in the future should also examine the possibility that corticosteroid treatment may have an adverse effect on visual outcome following optic nerve trauma.
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Document Type: Research Article

Affiliations: Restorative Neurology and Neuroscience 17: 157–163, 2000. Reprinted with permission from IOS Press.

Publication date: June 1, 2002

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