Affiliations: Orbital and Ophthalmic Plastic Surgery Division, Jules
Stein Eye Institute, Los Angeles, USA | Departments oflSurgery and Molecular & Medical
Pharmacology, Division of Neurosurgery and The Brain Research Institute, UCLA
School of Medicine, Los Angeles, USA
Note: [] Corresponding author: Dr. Steinsapir, 537 Newport Center Drive,
Suite 371, Newport Beach, CA 92660, USA. Tel.: +1 949 6319060, Fax: +1 949
6319070; E-mail: [email protected]
Abstract: Purpose: This study investigates the clinical dogma that very high
doses of methylprodnisolone 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.
Keywords: Corticosteroids, methylprednisolone, optic nerve injury, traumatic optic neuropathy, TON
