Kenneth D Steinsapir1, Robert A Goldberg. 1. Division of Orbital and Ophthalmic Plastic Surgery, Jules Stein Eye Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA 90025, USA. kenstein@ix.netcom.com
Abstract
PURPOSE: To critically review the treatment of traumatic optic neuropathy. DESIGN: A perspective of clinical and basic science studies related to traumatic optic neuropathy and its treatment. METHODS: Published clinical and basic science studies on traumatic optic neuropathy were critically reviewed and interpreted. RESULTS: Clinical progress in the treatment of traumatic optic neuropathy is limited by small clinical studies lacking appropriate control groups. The Corticosteroid Randomization for Acute Head Trauma (CRASH) trial found an increased rate of death among patients with acute head trauma treated with high-dose corticosteroids compared to placebo-treated patients (21% vs 18%, P = .0001). Recent animal studies also suggest that high-dose corticosteroids are toxic to the injured optic nerve. CONCLUSIONS: The Corticosteroid Randomization for Acute Head Trauma study is immediately relevant to the treatment of traumatic optic neuropathy as individuals with traumatic optic neuropathy often have concomitant head trauma. High-dose corticosteroids for traumatic optic neuropathy will result in a measurable loss of life in patients who also have a brain injury. Death has never been an endpoint for traumatic optic neuropathy studies. Given human and animal data suggesting that treatment is harmful and the lack of demonstrated clinical efficacy, corticosteroids should not be used to treat traumatic optic neuropathy. The benefit of optic canal decompression is also unclear. There is a need to identify traumatic optic neuropathy soon after injury to further define the natural history of this injury. This information will provide a basis for assessing potential future treatments for traumatic optic neuropathy.
PURPOSE: To critically review the treatment of traumatic optic neuropathy. DESIGN: A perspective of clinical and basic science studies related to traumatic optic neuropathy and its treatment. METHODS: Published clinical and basic science studies on traumatic optic neuropathy were critically reviewed and interpreted. RESULTS: Clinical progress in the treatment of traumatic optic neuropathy is limited by small clinical studies lacking appropriate control groups. The Corticosteroid Randomization for Acute Head Trauma (CRASH) trial found an increased rate of death among patients with acute head trauma treated with high-dose corticosteroids compared to placebo-treated patients (21% vs 18%, P = .0001). Recent animal studies also suggest that high-dose corticosteroids are toxic to the injured optic nerve. CONCLUSIONS: The Corticosteroid Randomization for Acute Head Trauma study is immediately relevant to the treatment of traumatic optic neuropathy as individuals with traumatic optic neuropathy often have concomitant head trauma. High-dose corticosteroids for traumatic optic neuropathy will result in a measurable loss of life in patients who also have a brain injury. Death has never been an endpoint for traumatic optic neuropathy studies. Given human and animal data suggesting that treatment is harmful and the lack of demonstrated clinical efficacy, corticosteroids should not be used to treat traumatic optic neuropathy. The benefit of optic canal decompression is also unclear. There is a need to identify traumatic optic neuropathy soon after injury to further define the natural history of this injury. This information will provide a basis for assessing potential future treatments for traumatic optic neuropathy.
Authors: U K Bodanapally; K Shanmuganathan; R K Shin; D Dreizin; L Katzman; R P Reddy; D Mascarenhas Journal: AJNR Am J Neuroradiol Date: 2015-04-16 Impact factor: 3.825