Traumatic Optic Neuropathy

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Abstract

Traumatic optic neuropathy (TON) refers to optic nerve injury resulting from direct and indirect head and facial trauma. The pathogenesis of indirect TON has not been fully elucidated, and the management of TON remains controversial. In this review article, I review the recent literature regarding TON and discuss how to manage indirect TON.

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Most cited references 30

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Final results of MRC CRASH, a randomised placebo-controlled trial of intravenous corticosteroid in adults with head injury-outcomes at 6 months.

Phil Edwards, Miguel Arango, Laura Balica … (2005)

MRC CRASH is a randomised controlled trial (ISRCTN74459797) of the effect of corticosteroids on death and disability after head injury. We randomly allocated 10,008 adults with head injury and a Glasgow Coma Scale score of 14 or less, within 8 h of injury, to a 48-h infusion of corticosteroid (methylprednisolone) or placebo. Data at 6 months were obtained for 9673 (96.7%) patients. The risk of death was higher in the corticosteroid group than in the placebo group (1248 [25.7%] vs 1075 [22.3%] deaths; relative risk 1.15, 95% CI 1.07-1.24; p=0.0001), as was the risk of death or severe disability (1828 [38.1%] vs 1728 [36.3%] dead or severely disabled; 1.05, 0.99-1.10; p=0.079). There was no evidence that the effect of corticosteroids differed by injury severity or time since injury. These results lend support to our earlier conclusion that corticosteroids should not be used routinely in the treatment of head injury.

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Erythropoietin as an antiapoptotic, tissue-protective cytokine.

M Brines, P. Ghezzi (2004)

Erythropoietin (EPO) increases the number of circulating erythrocytes primarily by preventing apoptosis of erythroid progenitors. In addition to this proerythroid action, results of recent studies show that systemically administered EPO is protective in vivo, in several animal models of neuronal injury. In vitro, EPO prevents neuronal apoptosis induced by a variety of stimuli. This review summarizes the neuroprotective actions of EPO and discusses the underlying mechanisms in terms of signal transduction pathways involved. The understanding of these mechanisms will help differentiate the neuroprotective actions of EPO from its role in the bone marrow.

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The treatment of traumatic optic neuropathy: the International Optic Nerve Trauma Study.

Amy Levin, Charles Beck, Ann Joseph … (1999)

To compare the visual outcome of traumatic optic neuropathy treated with corticosteroids, treated with optic canal decompression surgery, or observed without treatment. Comparative nonrandomized interventional study with concurrent treatment groups. A total of 133 patients with traumatic optic neuropathy (127 unilateral and 6 bilateral) who had an initial visual assessment within 3 days of injury. At least 1 month of follow-up was required for inclusion in the primary analysis. On the basis of treatment received within 7 days of injury, patients with unilateral injuries were categorized as being in one of three treatment groups: untreated (n = 9), corticosteroid (n = 85), or optic canal decompression surgery (n = 33). Visual acuity. Visual acuity increased by > or = 3 lines in 32% of the surgery group, 57% of the untreated group, and 52% of the steroid group (P = 0.22). The surgery group had more patients whose initial vision was no light perception. After adjustment for the baseline visual acuity, there were no significant differences between any of the treatment groups. There was no indication that the dosage or timing of corticosteroid treatment or the timing of surgery was associated with an increased probability of visual improvement. No clear benefit was found for either corticosteroid therapy or optic canal decompression surgery. The number of patients studied was sufficient to rule out major effects in the treatment groups, although clinically relevant effects in specific subgroups could have been missed. These results and the existing literature provide sufficient evidence to conclude that neither corticosteroids nor optic canal surgery should be considered the standard of care for patients with traumatic optic neuropathy. It is therefore clinically reasonable to decide to treat or not treat on an individual patient basis.

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Author and article information

Journal

Journal ID (nlm-ta): Korean J Neurotrauma

Journal ID (iso-abbrev): Korean J Neurotrauma

Journal ID (publisher-id): KJN

Title: Korean Journal of Neurotrauma

Publisher: Korean Neurotraumatology Society

ISSN (Print): 2234-8999

ISSN (Electronic): 2288-2243

Publication date (Print): April 2018

Publication date (Electronic): 30 April 2018

Volume: 14

Issue: 1

Pages: 1-5

Affiliations

Department of Ophthalmology, Soonchunhyang University Bucheon Hospital, Soonchunhyang University College of Medicine, Bucheon, Korea.

Author notes

Address for correspondence: Sun Young Jang. Department of Ophthalmology, Soonchunhyang University Bucheon Hospital, Soonchunhyang University College of Medicine, 170 Jomaru-ro, Bucheon 14584, Korea. Tel: +82-32-621-6718, Fax: +82-32-621-5018, ysyat01@ 123456naver.com

Article

DOI: 10.13004/kjnt.2018.14.1.1

PMC ID: 5949516

PubMed ID: 29774191

SO-VID: c923e22f-c764-4b39-825b-c36a2f09fbc5

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

History

Date received : 26 February 2018

Date revision received : 03 April 2018

Date accepted : 05 April 2018

Funding

Funded by: National Research Foundation of Korea, CrossRef http://dx.doi.org/10.13039/501100003725;

Award ID: NRF-2017R1A1A1A05001051

Funded by: Soonchunhyang University, CrossRef http://dx.doi.org/10.13039/501100002560;

Traumatic Optic Neuropathy

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Most cited references 30

Final results of MRC CRASH, a randomised placebo-controlled trial of intravenous corticosteroid in adults with head injury-outcomes at 6 months.

Erythropoietin as an antiapoptotic, tissue-protective cytokine.

The treatment of traumatic optic neuropathy: the International Optic Nerve Trauma Study.

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