Methylprednisolone exacerbates axonal loss following optic nerve trauma inrats

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 traumati c crush followed 30 minutes later by one of five intravenous treatments (me thylprednisolone 30 mg/kg, 60 mg/kg, 90 mg/kg, 120 mg/kg, or saline). Treat ment was continued for three additional administrations at 6 hour intervals . Untreated sham controls (n = 7) were also prepared. 'Six weeks after inju ry, animals were sacrificed, perfused and optic nerves systematically count ed. 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 m g/kg = 6,149 +/- 3,487 (n = 6). Consequently, the data revealed that saline treated animals retained more axons than those that were administered meth ylprednisolone (p < 0.02). Conclusions: We conclude that methylprednisolone exacerbates axonal loss fo llowing crush injury in the rat optic nerve. Based on the results of this s tudy, clinical studies of traumatic optic neuropathy in the future should a lso examine the possibility that corticosteroid treatment may have an adver se effect on visual outcome following optic nerve trauma.