NEURO-OPHTHALMOLOGY 2016, VOL. 40, NO. 4, 188–191 http://dx.doi.org/10.1080/01658107.2016.1177091
CASE REPORT
Optic Neuropathy with Delayed Onset After Trauma: Case Report and Review of the Literature Kai B. Kanga, Scott Jonesa, Amjad Ahmada, and Heather E. Mossa,b a
Illinois Eye and Ear Infirmary, Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago, Chicago, Illinois, USA; Department of Neurology and Rehabilitation, University of Illinois at Chicago, Chicago, Illinois, USA
b
ABSTRACT
ARTICLE HISTORY
The authors report a case of a 16-year-old healthy male who experienced loss of vision in the right eye immediately after getting punched by a fist. His visual acuity improved to 20/20 within hours, and the optic nerve head appeared normal. Computed tomography (CT) scan of the orbits showed fractures of the right inferior orbital wall and lamina papyracea. The morning after the injury, he awoke with right eye vision decline to count fingers. There was pallid optic nerve swelling. Magnetic resonance imaging (MRI) scan of the orbits showed right medial rectus enlargement and no optic canal abnormalities. The patient was treated with intravenous (IV) methylprednisolone with improvement in visual acuity. Literature of delayed traumatic optic neuropathy (TON) and anterior TON is reviewed.
Received 17 March 2016 Revised 7 April 2016 Accepted 7 April 2016 KEYWORDS
Optic neuropathy; steroid; trauma
Introduction
Case presentation
Traumatic optic neuropathy (TON) has an incidence of 0.7% to 2.5% following blunt or penetrating head injuries.1 The clinical presentation is one of immediate or delayed vision loss following injury with symptoms and signs of optic neuropathy, including vision loss, color vision deficits, relative afferent pupillary defect (except in bilateral symmetric cases), and lack of other findings on ophthalmic examination to account for the vision loss. Our case illustrates two distinct phases of TON uniquely occurring in the same individual with two distinct mechanisms; one of immediate posterior optic neuropathy likely as a result of indirect transmission of force to the optic canal, which resolved, and subsequent delayed anterior optic neuropathy likely due to ischaemia. This case illustrates that two mechanisms and locations can occur in the same patient and reinforces the importance of monitoring for delayed vision loss following blunt orbital trauma. The authors complied with the rules and regulations of the Health Insurance Portability and Accountability Act throughout the preparation of this article.
A 16-year-old otherwise healthy male noticed decreased vision in the right eye immediately after sustaining a closed fist injury to the eye. Over the next few hours, his central vision improved, but peripheral vision remained compromised. Ophthalmic findings 3 hours after the injury included visual acuity of 20/20 OU, no relative afferent pupillary defect (RAPD), mild right periorbital oedema and ecchymosis, and a 1-cm superficial skin laceration on the right upper eyelid. Fundus examination at that time showed normal-appearing optic nerves bilaterally. Orbital computed tomography (CT) showed a fracture of the right inferior orbital wall and lamina papyracea with minimal herniation of orbital contents, without fracture of the optic canal or intracanalicular haematoma. The next day, he awoke with worsening vision in the right eye and returned to the hospital for examination. He denied any secondary trauma to the eye after the initial trauma 1 day earlier. At this time, the patient’s visual acuity had worsened to count fingers OD, whereas OS remained unchanged. The patient was given 1 g of intravenous (IV)
CONTACT Heather E. Moss, MD, PhD [email protected] Illinois Eye and Ear Infirmary, Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago, 1855 W Taylor St, MC 648, Chicago, IL 60612, USA. © 2016 Taylor & Francis
NEURO-OPHTHALMOLOGY
solumedrol and transferred to our facility. On further examination, there was a RAPD OD, and confrontation visual fields were markedly constricted in this eye. External examination was unchanged, and intraocular pressures were normal. Again, there was no proptosis or restriction in eye movement. Anterior segment examination revealed only a small subconjunctival haemorrhage. Dilated fundus examination of the right eye (Figure 1) was notable for pallid diffuse optic nerve elevation, least pronounced temporally. Repeat orbital CT and magnetic resonance imaging (MRI) (Figure 2) was unchanged except for mild medial rectus enlargement.
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He was treated with 1 g of IV methylprednisolone daily for 3 days, followed by an oral steroid taper. Visual acuity improved to 20/100 OD on the second day of treatment and 20/25 OD on the third day of treatment. Goldmann visual field performed on the third day showed severe constriction, worse inferonasally and superotemporally (Figure 3a). At 2-month follow-up, he still had a afferent pupil defect (APD) but his visual acuity of the right eye was 20/20 without dyschromatopsia. Follow-up Goldmann visual field demonstrated nasal and inferior constriction, improved from prior (Figure 3b). Fundoscopic examination showed right optic atrophy. Discussion
Figure 1. Fundus photograph of the right eye illustrating diffuse optic disc elevation with pallor.
Figure 2. MRI of the orbit (axial T1) post-contrast demonstrating enlarged right medial rectus, intact optic canal, and a right posterior medial orbital wall fracture.
TON can be classified by region of optic nerve injury: anterior, characterised by optic nerve head swelling, or posterior, with normal-appearing optic nerve head in the acute setting. TON can result from direct mechanisms such as penetrating injury to the nerve, optic canal fracture, or compression in the optic canal or orbit. It can also result from indirect mechanisms, such as transmission of deformative stress forces through the orbital bones to the optic nerve in the optic canal following blunt trauma. In our case, the patient’s immediate vision loss may have been due to posterior optic neuropathy as a result of indirect transmission of force to the optic canal. This spontaneously improved, and he subsequently developed delayed anterior optic neuropathy likely due to ischaemia from compression by enlarged medial rectus muscle and/or direct effects of compression on ganglion cell function. He had improvement of visual acuity associated with high-dose IV steroid treatment. Delayed TON is less common than immediate TON, occurring in 13 cases (~10%) in the International Optic Nerve Trauma Study (IONTS).2 Delayed TON likely represents a heterogeneous group of mechanisms. Crowe and colleagues described a patient with vision loss starting 9 days after frontal head trauma due to haemorrhage and swelling within the optic nerve and chiasm.3 Eidlitz-Markus and colleagues also described a case of delayed TON that developed in a 16-year-old female 2 months after blunted
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K. B. KANG ET AL.
Figure 3. (a) Goldmann visual field of the right eye illustrating severe constriction, worse inferonasally and superotemporally. (b) Goldmann visual field of the right eye at 6-month follow-up illustrating nasal and inferior constriction, improved from prior.
head trauma. The authors were uncertain the mechanism for the optic neuropathy; however, pallid oedema of the optic disc was noted, suggesting an ischaemic mechanism, and the patient failed to respond to steroid treatment.4 In a case similar to ours, a woman experienced delayed vision to no light perception due to TON starting 3 days after blunt orbital injury. She had pallid swelling of optic nerve and delayed filling of the optic disc on fluorescein angiography, suggesting an ischaemic mechanism.5 In our case, delayed TON presenting upon awakening with anterior pallid disc swelling also suggests an ischaemic aetiology, perhaps due to compression of the posterior ciliary artery by the swollen medial rectus muscle. Nocturnal hypotension may have exacerbated hypoperfusion of the nerve head. Anterior TON, characterised by optic nerve head swelling, is less common than posterior TON. In a retrospective review describing the visual outcome of TON in 40 children and adolescents, Goldenberg-Cohen observed 6 (15%) to have optic disc oedema.6 Brodsky et al. illustrated the range of visual impairment from anterior TON in their description of three patients presenting with 20/20, 20/200, and light perception visual acuity.7 All three eyes were stricken by a foreign object. The authors observed that all three patients were young and two of the three had cup-less discs and proposed that in cup-less discs, oedematous thickening of the peripapillary sclera after blunt trauma may encroach upon a small scleral canal, leading to disruption of axonal transport, axonal crowding, and optic disc swelling.7 Non-traumatic causes of optic disc swelling include ischaemia,
inflammation, infiltration, and compression. Mechanistically, the first two are the most logical explanations for disc swelling in anterior TON. In our case and that published by Wyllie et al., the pallid disc swelling suggests an ischaemic aetiology.5 Treatment of TON using high-dose steroid stemmed from research and clinical practice in the treatment of spinal cord injuries. It has been shown that steroids exert a neuroprotective effect following trauma via their inhibition of free radical– induced lipid peroxidation and antioxidant properties.8–10 The IONTS demonstrated no clear benefit of corticosteroid therapy for TON.2 However, experts argue that TON likely represents a heterogeneous condition that includes subgroups of patients with optic neuropathy from various mechanisms of injury, such that it is difficult to predict which patient will benefit and who will not benefit from treatment.11–14 In the absence of a contraindication or significant risk, many clinicians continue to use steroids as treatment for TON. The IONTS was unable to make any inferences regarding the association between steroid treatment and outcome in delayed TON because most of these patients (9/13) received steroids. In two case series of anterior TON treated with steroids, 4/7 improved, 2/7 deteriorated, and 1/ 7, who had visual acuity of 20/20 at onset of therapy, was stable.6,7 We contribute an additional case on anterior TON demonstrating visual acuity improvement from count fingers to 20/20 associated with steroid administration. In our case, it is possible that steroids either decreased swelling of the rectus muscle, thus
NEURO-OPHTHALMOLOGY
mitigating hypoperfusion of the optic nerve head, or decreased ischaemic swelling within the optic nerve head. However, it is unknown if the patient could have recovered the same amount of vision if not treated with steroids. Traumatic optic neuropathy is a disease with variability in mechanism, timing of onset, pathophysiology, and resolution. Our case illustrates that two mechanisms and locations can occur in the same patient and reinforces the importance of monitoring for delayed vision loss following blunt orbital trauma. Steroid administration may be associated with recovery of vision, including in cases of delayed TON with anterior optic nerve injury. Funding This work was supported by Unrestricted Departmental Grant from Research to Prevent Blindness, National Institutes of Health grant K23-EY024345, and Research to Prevent Blindness Sybil B. Harrington Special Scholar Award.
References [1] Steinsapir K, Goldberg R. Traumatic Optic Neuropathy: A Critical Update. Medscape Web site. 2005 Comprehensive Ophthalmology Update. https://www.medscape.com/view article/501762. Accessed February 5 2016. [2] Levin LA, Beck RW, Joseph MP, Seiff S, Kraker R. The treatment of traumatic optic neuropathy: the International Optic Nerve Trauma Study. Ophthalmology 1999;106:1268–1277. [3] Crowe NW, Nickles TP, Troost BT, Elster AD. Intrachiasmal hemorrhage: a cause of delayed posttraumatic blindness. Neurology 1989;39:863–865. [4] Eidlitz-Markus T, Shuper A, Schwartz M, Mimouni M. Delayed post-traumatic visual loss: a clinical dilemma. Pediatr Neurol 2000;22:133–135.
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[5] Wyllie AM, McLeod D, Cullen JF. Traumatic ischemic optic neuropathy. Br J Ophthalmol 1972;56:851–853. [6] Goldenberg-Cohen N, Miller NR, Repka MX. Traumatic optic neuropathy in children and adolescents. J AAPOS 2004;8:20–27. [7] Brodsky MC, Wald KJ, Chen S, Weiter JJ. Protracted posttraumatic optic disc swelling. Ophthalmology 1995;102:1628–1631. [8] Young W, Flamm ES. Effect of high-dose corticosteroid therapy on blood flow, evoked potentials, and extracellular calcium in experimental spinal injury. J Neurosurg 1982;57:667–673. [9] Demopoulos HB, Flamm ES, Seligman ML, Pietronigro DD, Tomasula J, DeCrescito V. Further studies on free-radical pathology in the major central nervous system disorders: effect of very high doses of methylprednisolone on the functional outcome, morphology, and chemistry of experimental spinal cord impact injury. Can J Physiol Pharmacol 1982;60:1415–1424. [10] Bracken MB, Shepard MJ, Collins WF, Holford TR, Leo-Summers L, Baskin DS, Eisenberg HM, Flamm E, Leo-Summers L, Maroon J, et al. A randomized controlled trial of methylprednisolone or naloxone in the treatment of acute spinal cord injury. Results of the second national acute spinal cord injury study. N Engl J Med 1990;322:1405–1411. [11] Chou PI, Sadun AA, Chen YC, Su WY, Lin SZ, Lee CC. Clinical experiences in the management of traumatic optic neuropathy. Neuro-ophthalmology 1996;16:325–336. [12] Lee A. Traumatic optic neuropathy. Ophthalmology 2000;107:814. [13] Samardzic K, Samardzic J, Janjetovic Z, Samardzic I, Sekelj S, Latic-Hodzic L.. Traumatic optic neuropathy —to treat or to observe? Acta Inform Med 2012;20:131–132. [14] Hickman SJ, Tomsak RL. The treatment of indirect traumatic optic neuropathy with corticosteroids. Neuro-ophthalmology 2011;35:175–180.
CASE REPORT
Optic Neuropathy with Delayed Onset After Trauma: Case Report and Review of the Literature Kai B. Kanga, Scott Jonesa, Amjad Ahmada, and Heather E. Mossa,b a
Illinois Eye and Ear Infirmary, Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago, Chicago, Illinois, USA; Department of Neurology and Rehabilitation, University of Illinois at Chicago, Chicago, Illinois, USA
b
ABSTRACT
ARTICLE HISTORY
The authors report a case of a 16-year-old healthy male who experienced loss of vision in the right eye immediately after getting punched by a fist. His visual acuity improved to 20/20 within hours, and the optic nerve head appeared normal. Computed tomography (CT) scan of the orbits showed fractures of the right inferior orbital wall and lamina papyracea. The morning after the injury, he awoke with right eye vision decline to count fingers. There was pallid optic nerve swelling. Magnetic resonance imaging (MRI) scan of the orbits showed right medial rectus enlargement and no optic canal abnormalities. The patient was treated with intravenous (IV) methylprednisolone with improvement in visual acuity. Literature of delayed traumatic optic neuropathy (TON) and anterior TON is reviewed.
Received 17 March 2016 Revised 7 April 2016 Accepted 7 April 2016 KEYWORDS
Optic neuropathy; steroid; trauma
Introduction
Case presentation
Traumatic optic neuropathy (TON) has an incidence of 0.7% to 2.5% following blunt or penetrating head injuries.1 The clinical presentation is one of immediate or delayed vision loss following injury with symptoms and signs of optic neuropathy, including vision loss, color vision deficits, relative afferent pupillary defect (except in bilateral symmetric cases), and lack of other findings on ophthalmic examination to account for the vision loss. Our case illustrates two distinct phases of TON uniquely occurring in the same individual with two distinct mechanisms; one of immediate posterior optic neuropathy likely as a result of indirect transmission of force to the optic canal, which resolved, and subsequent delayed anterior optic neuropathy likely due to ischaemia. This case illustrates that two mechanisms and locations can occur in the same patient and reinforces the importance of monitoring for delayed vision loss following blunt orbital trauma. The authors complied with the rules and regulations of the Health Insurance Portability and Accountability Act throughout the preparation of this article.
A 16-year-old otherwise healthy male noticed decreased vision in the right eye immediately after sustaining a closed fist injury to the eye. Over the next few hours, his central vision improved, but peripheral vision remained compromised. Ophthalmic findings 3 hours after the injury included visual acuity of 20/20 OU, no relative afferent pupillary defect (RAPD), mild right periorbital oedema and ecchymosis, and a 1-cm superficial skin laceration on the right upper eyelid. Fundus examination at that time showed normal-appearing optic nerves bilaterally. Orbital computed tomography (CT) showed a fracture of the right inferior orbital wall and lamina papyracea with minimal herniation of orbital contents, without fracture of the optic canal or intracanalicular haematoma. The next day, he awoke with worsening vision in the right eye and returned to the hospital for examination. He denied any secondary trauma to the eye after the initial trauma 1 day earlier. At this time, the patient’s visual acuity had worsened to count fingers OD, whereas OS remained unchanged. The patient was given 1 g of intravenous (IV)
CONTACT Heather E. Moss, MD, PhD [email protected] Illinois Eye and Ear Infirmary, Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago, 1855 W Taylor St, MC 648, Chicago, IL 60612, USA. © 2016 Taylor & Francis
NEURO-OPHTHALMOLOGY
solumedrol and transferred to our facility. On further examination, there was a RAPD OD, and confrontation visual fields were markedly constricted in this eye. External examination was unchanged, and intraocular pressures were normal. Again, there was no proptosis or restriction in eye movement. Anterior segment examination revealed only a small subconjunctival haemorrhage. Dilated fundus examination of the right eye (Figure 1) was notable for pallid diffuse optic nerve elevation, least pronounced temporally. Repeat orbital CT and magnetic resonance imaging (MRI) (Figure 2) was unchanged except for mild medial rectus enlargement.
189
He was treated with 1 g of IV methylprednisolone daily for 3 days, followed by an oral steroid taper. Visual acuity improved to 20/100 OD on the second day of treatment and 20/25 OD on the third day of treatment. Goldmann visual field performed on the third day showed severe constriction, worse inferonasally and superotemporally (Figure 3a). At 2-month follow-up, he still had a afferent pupil defect (APD) but his visual acuity of the right eye was 20/20 without dyschromatopsia. Follow-up Goldmann visual field demonstrated nasal and inferior constriction, improved from prior (Figure 3b). Fundoscopic examination showed right optic atrophy. Discussion
Figure 1. Fundus photograph of the right eye illustrating diffuse optic disc elevation with pallor.
Figure 2. MRI of the orbit (axial T1) post-contrast demonstrating enlarged right medial rectus, intact optic canal, and a right posterior medial orbital wall fracture.
TON can be classified by region of optic nerve injury: anterior, characterised by optic nerve head swelling, or posterior, with normal-appearing optic nerve head in the acute setting. TON can result from direct mechanisms such as penetrating injury to the nerve, optic canal fracture, or compression in the optic canal or orbit. It can also result from indirect mechanisms, such as transmission of deformative stress forces through the orbital bones to the optic nerve in the optic canal following blunt trauma. In our case, the patient’s immediate vision loss may have been due to posterior optic neuropathy as a result of indirect transmission of force to the optic canal. This spontaneously improved, and he subsequently developed delayed anterior optic neuropathy likely due to ischaemia from compression by enlarged medial rectus muscle and/or direct effects of compression on ganglion cell function. He had improvement of visual acuity associated with high-dose IV steroid treatment. Delayed TON is less common than immediate TON, occurring in 13 cases (~10%) in the International Optic Nerve Trauma Study (IONTS).2 Delayed TON likely represents a heterogeneous group of mechanisms. Crowe and colleagues described a patient with vision loss starting 9 days after frontal head trauma due to haemorrhage and swelling within the optic nerve and chiasm.3 Eidlitz-Markus and colleagues also described a case of delayed TON that developed in a 16-year-old female 2 months after blunted
190
K. B. KANG ET AL.
Figure 3. (a) Goldmann visual field of the right eye illustrating severe constriction, worse inferonasally and superotemporally. (b) Goldmann visual field of the right eye at 6-month follow-up illustrating nasal and inferior constriction, improved from prior.
head trauma. The authors were uncertain the mechanism for the optic neuropathy; however, pallid oedema of the optic disc was noted, suggesting an ischaemic mechanism, and the patient failed to respond to steroid treatment.4 In a case similar to ours, a woman experienced delayed vision to no light perception due to TON starting 3 days after blunt orbital injury. She had pallid swelling of optic nerve and delayed filling of the optic disc on fluorescein angiography, suggesting an ischaemic mechanism.5 In our case, delayed TON presenting upon awakening with anterior pallid disc swelling also suggests an ischaemic aetiology, perhaps due to compression of the posterior ciliary artery by the swollen medial rectus muscle. Nocturnal hypotension may have exacerbated hypoperfusion of the nerve head. Anterior TON, characterised by optic nerve head swelling, is less common than posterior TON. In a retrospective review describing the visual outcome of TON in 40 children and adolescents, Goldenberg-Cohen observed 6 (15%) to have optic disc oedema.6 Brodsky et al. illustrated the range of visual impairment from anterior TON in their description of three patients presenting with 20/20, 20/200, and light perception visual acuity.7 All three eyes were stricken by a foreign object. The authors observed that all three patients were young and two of the three had cup-less discs and proposed that in cup-less discs, oedematous thickening of the peripapillary sclera after blunt trauma may encroach upon a small scleral canal, leading to disruption of axonal transport, axonal crowding, and optic disc swelling.7 Non-traumatic causes of optic disc swelling include ischaemia,
inflammation, infiltration, and compression. Mechanistically, the first two are the most logical explanations for disc swelling in anterior TON. In our case and that published by Wyllie et al., the pallid disc swelling suggests an ischaemic aetiology.5 Treatment of TON using high-dose steroid stemmed from research and clinical practice in the treatment of spinal cord injuries. It has been shown that steroids exert a neuroprotective effect following trauma via their inhibition of free radical– induced lipid peroxidation and antioxidant properties.8–10 The IONTS demonstrated no clear benefit of corticosteroid therapy for TON.2 However, experts argue that TON likely represents a heterogeneous condition that includes subgroups of patients with optic neuropathy from various mechanisms of injury, such that it is difficult to predict which patient will benefit and who will not benefit from treatment.11–14 In the absence of a contraindication or significant risk, many clinicians continue to use steroids as treatment for TON. The IONTS was unable to make any inferences regarding the association between steroid treatment and outcome in delayed TON because most of these patients (9/13) received steroids. In two case series of anterior TON treated with steroids, 4/7 improved, 2/7 deteriorated, and 1/ 7, who had visual acuity of 20/20 at onset of therapy, was stable.6,7 We contribute an additional case on anterior TON demonstrating visual acuity improvement from count fingers to 20/20 associated with steroid administration. In our case, it is possible that steroids either decreased swelling of the rectus muscle, thus
NEURO-OPHTHALMOLOGY
mitigating hypoperfusion of the optic nerve head, or decreased ischaemic swelling within the optic nerve head. However, it is unknown if the patient could have recovered the same amount of vision if not treated with steroids. Traumatic optic neuropathy is a disease with variability in mechanism, timing of onset, pathophysiology, and resolution. Our case illustrates that two mechanisms and locations can occur in the same patient and reinforces the importance of monitoring for delayed vision loss following blunt orbital trauma. Steroid administration may be associated with recovery of vision, including in cases of delayed TON with anterior optic nerve injury. Funding This work was supported by Unrestricted Departmental Grant from Research to Prevent Blindness, National Institutes of Health grant K23-EY024345, and Research to Prevent Blindness Sybil B. Harrington Special Scholar Award.
References [1] Steinsapir K, Goldberg R. Traumatic Optic Neuropathy: A Critical Update. Medscape Web site. 2005 Comprehensive Ophthalmology Update. https://www.medscape.com/view article/501762. Accessed February 5 2016. [2] Levin LA, Beck RW, Joseph MP, Seiff S, Kraker R. The treatment of traumatic optic neuropathy: the International Optic Nerve Trauma Study. Ophthalmology 1999;106:1268–1277. [3] Crowe NW, Nickles TP, Troost BT, Elster AD. Intrachiasmal hemorrhage: a cause of delayed posttraumatic blindness. Neurology 1989;39:863–865. [4] Eidlitz-Markus T, Shuper A, Schwartz M, Mimouni M. Delayed post-traumatic visual loss: a clinical dilemma. Pediatr Neurol 2000;22:133–135.
191
[5] Wyllie AM, McLeod D, Cullen JF. Traumatic ischemic optic neuropathy. Br J Ophthalmol 1972;56:851–853. [6] Goldenberg-Cohen N, Miller NR, Repka MX. Traumatic optic neuropathy in children and adolescents. J AAPOS 2004;8:20–27. [7] Brodsky MC, Wald KJ, Chen S, Weiter JJ. Protracted posttraumatic optic disc swelling. Ophthalmology 1995;102:1628–1631. [8] Young W, Flamm ES. Effect of high-dose corticosteroid therapy on blood flow, evoked potentials, and extracellular calcium in experimental spinal injury. J Neurosurg 1982;57:667–673. [9] Demopoulos HB, Flamm ES, Seligman ML, Pietronigro DD, Tomasula J, DeCrescito V. Further studies on free-radical pathology in the major central nervous system disorders: effect of very high doses of methylprednisolone on the functional outcome, morphology, and chemistry of experimental spinal cord impact injury. Can J Physiol Pharmacol 1982;60:1415–1424. [10] Bracken MB, Shepard MJ, Collins WF, Holford TR, Leo-Summers L, Baskin DS, Eisenberg HM, Flamm E, Leo-Summers L, Maroon J, et al. A randomized controlled trial of methylprednisolone or naloxone in the treatment of acute spinal cord injury. Results of the second national acute spinal cord injury study. N Engl J Med 1990;322:1405–1411. [11] Chou PI, Sadun AA, Chen YC, Su WY, Lin SZ, Lee CC. Clinical experiences in the management of traumatic optic neuropathy. Neuro-ophthalmology 1996;16:325–336. [12] Lee A. Traumatic optic neuropathy. Ophthalmology 2000;107:814. [13] Samardzic K, Samardzic J, Janjetovic Z, Samardzic I, Sekelj S, Latic-Hodzic L.. Traumatic optic neuropathy —to treat or to observe? Acta Inform Med 2012;20:131–132. [14] Hickman SJ, Tomsak RL. The treatment of indirect traumatic optic neuropathy with corticosteroids. Neuro-ophthalmology 2011;35:175–180.
