AUTHOR AND EDITOR INFORMATION

Section 1 of 9  

• Authors and Editors
• Introduction
• Relevant Anatomy
• Workup
• Treatment
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

INTRODUCTION

Section 2 of 9  

• Authors and Editors
• Introduction
• Relevant Anatomy
• Workup
• Treatment
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Traumatic optic neuropathy (TON) refers to an acute injury of the optic nerve secondary to trauma. The optic nerve axons may be damaged either directly or indirectly and the visual loss may be partial or complete. An indirect injury to the optic nerve typically occurs from the transmission of forces to the optic canal from blunt head trauma. This is in contrast to direct TON, which results from an anatomical disruption of the optic nerve fibers from penetrating orbital trauma, bone fragments within the optic canal, or nerve sheath hematomas. 

Problem

Patients with TON can present with a variable degree of vision loss (decreased visual acuity, visual field abnormalities, or loss of color vision). Most cases (up to 60%) present with severe vision loss of light perception (LP) or worse. In the acute phase, the optic nerve usually appears normal on funduscopic examination, but optic nerve atrophy is often seen 3-6 weeks after the injury.

Frequency

The incidence of TON in the setting of a closed traumatic head injury in various studies ranges from 0.5-5%. The vast majority of TON cases are seen in males (up to 85%), with a mean age of 34 years. Motor vehicle and bicycle accidents account for the majority of causes, followed by falls and assaults. TON has also been associated with penetrating orbital trauma (eg, stab wounds, pellet and gunshot wounds, foreign bodies) and recreational sports (eg, paint ball injury).   

Pathophysiology

The pathophysiology of TON is thought to be multifactorial, and some researchers have also postulated a primary and secondary mechanism of injury. In indirect TON cases, the injury to the axons is thought to be induced by shearing forces that are transmitted to the fibers or to the vascular supply of the nerve. Studies have shown that forces applied to the frontal bone and malar eminences are transferred and concentrated in the area near the optic canal. The tight adherence of the optic nerve’s dural sheath to the periosteum within the optic canal is also thought to contribute to this segment of the nerve being extremely susceptible to the deformative stresses of the skull bones. Such injury leads to ischemic injury to the retinal ganglion cells within the optic canal.

A secondary mechanism can result in optic nerve swelling after the occurrence the acute injury. The optic nerve swelling can exacerbate retinal ganglion cell degeneration by further compromising the vascular blood supply, either through a rise in intraluminal pressure or reactive vasospasm. These secondary mechanisms, in theory, form the rationale for optic canal decompression via medical (ie, steroids) or surgical means (ie, bony decompression). Finally, the intracranial segment of the optic nerve may be damaged by forces delivered to the axons by the shifting of the brain following head trauma. With this mechanism, the nerve fibers may be injured against the falciform dural fold or through a shearing force where the nerve becomes fixed as it enters the intracranial opening of the optic foramen.

RELEVANT ANATOMY

Section 3 of 9  

• Authors and Editors
• Introduction
• Relevant Anatomy
• Workup
• Treatment
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

The human orbit is composed of seven bones that comprise 4 walls: the roof, lateral wall, medial wall, and floor. The 7 bones include: ethmoid, frontal, lacrimal, maxillary, palatine, sphenoid (lesser and greater wings), and zygomatic bones. The 4 orbital walls converge posteriorly at the apex of the orbit, and the optic canal is located within the lesser wing of the sphenoid, which is one of the bones that comprise the orbital roof. 

The optic canal is separated from the superior orbital fissure by the optic strut of the sphenoid bone; hence the optic strut comprises the optic canal's lateral wall. The canal's medial wall separates it from the sphenoid sinus. Structures that pass through the optic canal include the optic nerve sheath and axons, their supportive glia, the ophthalmic artery, and branches of the carotid sympathetic plexus of the autonomic nervous system.

Throughout its intraorbital course, the optic nerve remains surrounded by pia, arachnoid, and dura mater, which move along with the optic nerve during normal eye movements. Within the optic canal, the sheath of the optic nerve is fused to the sphenoid periosteum, and, as a result, the nerve and its sheath are tightly fixed to the bony canal within this confined space. At the posterior foramen of the optic canal, the optic nerve sheath fuses with an overlying falciform fold of dura that lines the calvaria.

Pial branches of the internal carotid, anterior cerebral, and anterior communicating arteries perfuse the intracranial optic nerve. Small pial branches from the ophthalmic artery supply the intracanalicular optic nerve. The intraorbital optic nerve is also supplied by perforating branches derived from the ophthalmic artery. The arterial circle of Zinn-Haller supplies the intraocular optic nerve with contributions from the posterior ciliary arteries, the pial arterial network, and the peripapillary choroidal vasculature.

WORKUP

Section 4 of 9  

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• Introduction
• Relevant Anatomy
• Workup
• Treatment
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Imaging Studies

Neuroimaging studies (CT scanning or MRI) are an important part of the assessment when TON is suspected. In the post-trauma setting, CT scanning is the preferred modality for demonstrating the presence of an optic canal fracture, a displaced bony fragment impinging upon the optic nerve, a metallic foreign body in the orbit, orbital emphysema, or an optic nerve sheath hematoma. A brain and orbit MRI may be useful in certain settings to delineate the extent of hemorrhage involving the neurovascular structures at the orbital apex or to rule out inflammatory or infiltrative causes for an optic neuropathy. The vast majority of patients with TON suffer an indirect injury to the optic nerve within the optic canal, and neuroimaging studies typically demonstrate no abnormalities of the anterior visual pathways, although a fracture in the region of the optic canal may be seen.

Other Tests

• Visual field perimetry
• • Automated perimetry can be obtained only in patients who retain adequate vision/acuity. Patients with poor visual acuity (worse than 20/200) may be assessed with Goldmann perimetry or with confrontational visual field testing. 
  • No visual field loss pattern is pathognomonic for traumatic optic neuropathy (TON), although a dense central scotoma is characteristic. Recovery of optic nerve function may be documented via serial visual field testing.
• Visual evoked potential (VEP)
• • VEP can be helpful to document the presence of TON in unresponsive patients or in cases with concomitant ocular injuries. Patients can also be followed with serial VEP examinations to document recovery of function when clinical parameters are equivocal.
  • VEP is not considered essential in making the diagnosis of TON, and logistically, the ability to perform a neurophysiological evaluation is often hindered by the inability to transport the trauma patient to the neurophysiology laboratory.
  • In unilateral cases of TON, a flash VEP amplitude ratio (affected side/normal side) greater than 0.5 appears predictive of a favorable, long-term visual outcome. Visual recovery is considered unlikely when VEP amplitudes are nonrecordable.
• Retinal nerve fiber layer (NFL) imaging: Scanning laser polarimetry and optical coherence tomography can be used to assess and monitor retinal NFL axonal loss during the period of follow-up.

Diagnostic Procedures

TON is based on a clinical diagnosis of optic nerve dysfunction supported by a recent history of trauma to the head. In an acute setting following trauma, the diagnosis may be delayed if the patient is unconscious and a formal visual acuity assessment cannot be performed. In a conscious, cooperative patient, the diagnosis of TON should be verified by testing the patient for an abnormal visual acuity, an ipsilateral afferent pupillary defect (APD), impairment of color vision, and a visual field defect on formal perimetry.

Visual acuity

Even in an acute trauma setting, patients should have a visual acuity assessment as soon as possible. This can be performed with a Snellen eye chart (which measures distance vision) or a near vision card. If the patient cannot read the top letter on the eye chart, the visual acuity may be recorded with the following nomenclature (in order of decreasing visual acuity): counting fingers vision, hand motion perception, light perception (LP), or no light perception (NLP).
 
Pupil examination

The pupil examination assesses the size of both pupils, the response of the pupils to light and near stimulation, and an evaluation for a relative afferent pupillary defect or APD (swinging-flashlight test). The swinging-flashlight test compares the pupillary reaction to light between the two eyes; normally, both pupils should constrict equally to light, and the constriction should be maintained as the light is rapidly switched between the two pupils. An eye with a unilateral optic nerve injury will demonstrate an APD, verifying the presence of TON. In the rare case of a bilateral TON, a relative APD may not be seen if the injury is symmetric between the 2 sides, and both pupils may be dilated and nonreactive to light if the injury is profound.
 
Funduscopic examination   

The funduscopic examination can be performed with the use of a direct ophthalmoscope, indirect ophthalmoscope, or the slit-lamp biomicroscope. Because the location of the injury in most TON cases is within the posterior orbit or the optic canal, the optic disc typically appears normal on funduscopic examination on initial diagnosis. Optic nerve atrophy usually appears 3-4 weeks after the traumatic event, and the disc acquires a diffuse pallor. Rarely, optic nerve changes can be seen with direct injuries to the retrobulbar section of the optic nerve, presenting as an avulsed optic nerve head or optic disc swelling with surrounding hemorrhage.  

Histologic Findings

Cadaver studies have not demonstrated consistent histopathologic findings in traumatic optic neuropathy, suggesting multiple mechanisms of injury in patients with TON. Gross pathologic changes that have been reported include hematomas within the optic nerve sheath and occasionally areas of visible necrosis. Microscopic findings include interstitial hemorrhage, fibrosis of the pial septa, and a chronic inflammatory infiltrate by lymphocytes, plasma cells, and iron-laden macrophages. One case demonstrated degeneration of axons with loss of myelin in a triangular section consistent with damage to the penetrating vessels supplying the infracted region. With time, loss of astrocyte support appears to occur within the optic nerve in TON injuries, followed by replacement of the axons with microglia. Based on the histopathologic findings in TON, axonal loss appears to occur either through shearing forces, hemorrhagic infarction, direct compression of the nerve fibers from an extrinsic nerve sheath hematoma, or a combination of these mechanisms.

TREATMENT

Section 5 of 9  

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• Introduction
• Relevant Anatomy
• Workup
• Treatment
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Medical therapy

The main treatment options for traumatic optic neuropathy (TON) include systemic corticosteroids and surgical optic nerve decompression, either alone or in combination. Review and analysis of the literature are complicated by the variety of therapeutic approaches and a lack of randomized, controlled studies on the use of these modalities for TON.

The current knowledge base on the use of steroids for TON is based on small retrospective studies, anecdotal reports, and extrapolation from national traumatic brain and spinal cord injury studies. Steroid therapy for TON can be categorized as follows: moderate dose (60-100mg of oral prednisolone), high dose (1 gram of intravenous methylprednisolone/day), or mega dose (30 mg/kg loading dose of intravenous methylprednisone, followed by 5.4 mg/kg/h for 24 hours).

Steroids have been used in TON since the early 1980s because of their perceived benefits in various animal models of central nervous system injury.  Steroids were thought to provide neuroprotection in traumatic central nervous system injury through their antioxidant properties and inhibition of free radical-induced lipid peroxidation.

In 1990, Bracken and colleagues published their findings on the use of mega dose corticosteroid therapy in the National Acute Spinal Cord Injury Study 2 (NASCIS 2).¹ The NASCIS 2 was a multicenter clinical trial that evaluated patients with acute spinal cord injury treated with placebo, methylprednisolone, or naloxone. The study showed that methylprednisolone (30 mg/kg loading dose, followed by 5.4 mg/kg/h for 24 hours) started within 8 hours of injury was associated with a significant improvement in both motor and sensory function compared with patients treated with a placebo.

The findings of the NASCIS trials significantly influenced clinical practice and led to an increased use of steroids in treating TON. However, the clinical improvement was modest in these studies, and concern existed that the clinical benefit demonstrated for those patients treated in the first eight hours with mega dose steroids was the result of a statistical bias, since the analysis was performed post hoc rather than prospectively.

In 2005, the results of the Corticosteroid Randomization After Significant Head Injury (CRASH) trial raised concerns regarding the use of mega dose steroids (same dose as given in the NASCIS 2 study) in traumatic brain injury.² This study was the largest randomized study that evaluated steroids in patients with traumatic brain injury and was stopped early due to the significantly increased risk of death in patients that received mega dose steroids at their 6-month follow-up when compared with the placebo group (25.7% vs 22.3%; RR 1.15 CI 1.07 to 1.24; p=0.0001). Although the etiology of the increased risk of death was not determined, the findings of this study should be taken into consideration when managing cases of TON with concurrent traumatic brain injury.

Furthermore, concerns have been raised regarding the extrapolation of data from spinal cord injury studies to TON. There are important histologic distinctions between the spinal cord and optic nerve; for example, the optic nerve is a pure white matter tract and the spinal cord is a mixed gray and white matter tract. As a result, significant biologic differences may exist between the repair mechanisms of the optic nerve axons and insults to the spinal cord.

The International Optic Nerve Trauma Study (IONTS) was a nonrandomized intervention trial that compared visual outcomes for patients with TON treated with observation, systemic steroids, or optic canal decompression.³ Published in 1999, the study included 133 patients who were evaluated and treated within 7 days of the traumatic event, with most of the patients being treated with either corticosteroids (n=85) or surgical decompression of the optic canal (n=33). Follow-up results showed that visual acuity increased by more than 3 lines in 32% of the surgery group, 52% of the corticosteroid group, and 57% of the observation group. However, the study was nonrandomized and uncontrolled, and the small numbers of patients in the observation group (n=9) limited the strength of the study’s statistical power.

Recent animal studies have also found variable results with steroid therapy. These animal models involve a direct, crush injury mechanism for inducing TON in rats, and any extrapolation of the data to humans with indirect insults to the optic nerve must be made with caution. However, no study has demonstrated a beneficial effect for steroid therapy in animals with TON, and one study, in particular, found that steroids exacerbated axonal loss as evidenced by a dose-dependent decline in axonal counts with increasing doses of steroids.⁴ Such findings may suggest that steroids can exert a negative effect on ganglion cell survival, especially at higher, mega dose levels, due to their suppression of endogenous neuroprotective pathways.

Based on the current evidence, a therapeutic role for corticosteroids in the management of TON is unsubstantiated. If steroids are considered for TON, they should not be used in cases with concomitant traumatic brain injury or in patients that present 8 hours or more after initial injury. Whether clinicians should use mega dose rather than lower doses of steroids for selected cases of TON is also not clearly defined by the literature. The NASCIS studies used mega dose steroids in their protocol to demonstrate a beneficial effect in a subset of their patients, but the CRASH study identified several serious complications associated with their use in the trauma setting. Additionally, animal studies have demonstrated an association between increasing doses of steroids and retinal ganglion cell death.^{5, 6, 7}

Surgical therapy

The rationale for surgical therapy in indirect TON is to decompress the optic nerve at the site of injury, which is often the intracanalicular segment. Surgical decompression is thought to help reduce optic nerve compression and subsequent vascular compromise that may occur as a result of the indirect injury. Additionally, surgery has been postulated to remove bone fragments that may be impinging on the optic nerve within the optic canal.

However, no randomized, controlled studies have been performed to evaluate the role of surgery in TON. As mentioned previously, one of the largest series is from the IONTS, which did not provide any convincing evidence that surgical decompression of the optic canal in TON is superior to observation or corticosteroid therapy. Additionally, in cases in which bony fragments are impinging on the optic nerve within the canal, the prognosis of visual recovery is extremely poor because the bony fragments are more likely to have anatomically disrupted the optic nerve axons, leading to irreversible visual loss.

Interpreting the efficacy of surgical decompression when reviewing the published studies is difficult because they consist of small, retrospective series that have variable methodologies and inclusion criteria (ie, degree of vision loss, timing of surgery, whether concomitant steroids were used). In addition, the probability of selection bias for TON patients who elect to have surgical decompression cannot be ignored because patients with the worse visual function at presentation or those who have failed steroid therapy tend to be included in these surgical series. The timing of surgery and the preferred surgical approach is also controversial.

The variety of surgical approaches used in optic nerve decompression include intracranial, extracranial, orbital, transethmoidal, endonasal, and sublabial approaches, and the selection of the technique tends to be based on the surgeon’s training, background, and experience. Patients with profound vision loss and a visualized bone fragment impinging on a segment of the intracanalicular optic nerve on neuroimaging have been considered to be the best candidates for surgical intervention. Although anecdotal reports of impressive visual recovery exist for such patients, most cases with direct injuries to the optic nerve do not improve, and the risk of possible surgical complications such as cerebrospinal fluid leak or postoperative bleeding cannot be ignored.

OUTCOME AND PROGNOSIS

Section 6 of 9  

• Authors and Editors
• Introduction
• Relevant Anatomy
• Workup
• Treatment
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Most studies show a significant association between initial and final visual acuities. Patients with no light perception (NLP) likely have little to no recovery in vision.  However, studies show that up to 50% of patients with traumatic optic neuropathy (TON) can have some improvement in vision, with or without treatment, although most of the time improvement is minimal. No well-designed study has shown whether surgical decompression or steroids has any better outcome than observation alone. In fact, the rate of minimal but spontaneous visual improvement in indirect TON is relatively high, ranging from 20-57% in published series.
 
Studies have shown that TON with concomitant orbital fractures tends to have more severe visual loss.^{8, 9} Up to 85% of the patients with an orbital fracture (29 out of 34) presented with NLP in one particular study.⁹ The presence of an orbital fracture implies a greater transmission of force to the optic canal, and hence, a greater injury to the optic nerve.

FUTURE AND CONTROVERSIES

Section 7 of 9  

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• Introduction
• Relevant Anatomy
• Workup
• Treatment
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Traumatic optic neuropathy (TON) can lead to profound visual loss from either indirect or direct mechanisms. The diagnosis can be made with accurate history taking and clinical examination, based on the presence of visual loss (with accompanying loss of color vision and possible visual field defects) and an accompanying relative afferent pupillary defect (APD).

The optimal treatment for TON, however, remains debated among physicians. A review of the available literature, especially the IONTS and CRASH studies, provides insufficient evidence to conclude that corticosteroid therapy and/or optic canal surgery provides a therapeutic benefit over observation alone in patients with TON. Patients with TON treated with systemic steroids appear to have similar rates of visual recovery as untreated patients, and both animal and human studies suggest that under certain conditions, systemic steroids may actually be harmful, particularly at higher doses.

Therefore, corticosteroids should not be used in cases with concomitant traumatic brain injury or in patients who present 8 hours or more after initial injury. Based on the available evidence, surgical decompression of the optic canal in cases is not routinely recommended in TON. If treatment with either steroids or surgical intervention is considered, appropriate counseling should be given to the patient and their family about their potential benefits and risks in order to help them make an informed decision. 
 

MULTIMEDIA

Section 8 of 9  

• Authors and Editors
• Introduction
• Relevant Anatomy
• Workup
• Treatment
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Media file 1:  Plain film radiograph of a 2-year-old girl following blunt periocular trauma. Although a left orbital wall fracture is not evident, a loculated pocket of intraorbital air is highlighted by the arrow.
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Media type:  X-RAY

Media file 2:  Note the proptosis induced by the large accumulation of intraorbital emphysema. Also, note the relatively nondisplaced nature of the medial orbital wall fracture. This patient experienced a threatened central retinal artery obstruction due to this condition. Evacuation of the orbital air relieved the compromised retinal circulation.
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Media type:  CT

Media file 3:  Fundus photograph of a 24-year-old man with vision loss following blunt periocular trauma. The incident occurred during a baseball game when the patient (a base runner) collided with the catcher. The area of opacification extending from the temporal aspect of the optic nerve head represents retinal ischemia and is indicative of an anterior ischemic optic nerve injury. Such injuries may have a better long-term visual prognosis than posterior ischemic optic neuropathies. Indirect traumatic optic neuropathy more commonly results in posterior optic nerve injuries. Posterior injuries usually do not result in any morphologic change to the optic nerve head appearance.
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Media type:  Photo

Media file 4:  Axial CT scan of the orbit. Note the mildly displaced fracture at the junction of the posterior medial orbital wall and optic canal.
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Media type:  CT

Media file 5:  Fundus photograph of the left eye in a 33-year-old male who suffered a severe head injury after falling off a ladder one year prior to presenting to our clinic. The patient has a visual acuity of counting fingers (CF) of 6 feet in his left eye and a large relative afferent pupillary defect. Note the optic nerve's pale appearance.
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Media type:  Image

REFERENCES

Section 9 of 9

• Authors and Editors
• Introduction
• Relevant Anatomy
• Workup
• Treatment
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

1. Bracken MB, Shepard MJ, Collins WF, 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. May 17 1990;322(20):1405-11. [Medline].
2. Edwards P, Arango M, Balica L, et al. Final results of MRC CRASH, a randomised placebo-controlled trial of intravenous corticosteroid in adults with head injury-outcomes at 6 months. Lancet. Jun 4-10 2005;365(9475):1957-9. [Medline].
3. Levin LA, Beck RW, Joseph MP, et al. The treatment of traumatic optic neuropathy: the International Optic Nerve Trauma Study. Ophthalmology. Jul 1999;106(7):1268-77. [Medline].
4. Steinsapir KD. Treatment of traumatic optic neuropathy with high-dose corticosteroid. J Neuroophthalmol. Mar 2006;26(1):65-7. [Medline].
5. Steinsapir KD, Goldberg RA, Sinha S, et al. Methylprednisolone exacerbates axonal loss following optic nerve trauma in rats. Restor Neurol Neurosci. 2000;17(4):157-163. [Medline].
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9. Wang BH, Robertson BC, Girotto JA, et al. Traumatic optic neuropathy: a review of 61 patients. Plast Reconstr Surg. Jun 2001;107(7):1655-64. [Medline].
10. Bracken MB, Shepard MJ, Holford TR, et al. Administration of methylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hours in the treatment of acute spinal cord injury. Results of the Third National Acute Spinal Cord Injury Randomized Controlled Trial. National Acute Spinal Cord Injury Study. JAMA. May 28 1997;277(20):1597-604. [Medline].
11. Carta A, Ferrigno L, Salvo M, et al. Visual prognosis after indirect traumatic optic neuropathy. J Neurol Neurosurg Psychiatry. Feb 2003;74(2):246-8. [Medline].
12. Girard BC, Bouzas EA, Lamas G, et al. Visual improvement after transethmoid-sphenoid decompression in optic nerve injuries. J Clin Neuroophthalmol. Sep 1992;12(3):142-8. [Medline].
13. Goldberg RA, Steinsapir KD. Extracranial optic canal decompression: indications and technique. Ophthal Plast Reconstr Surg. Sep 1996;12(3):163-70. [Medline].
14. Goldenberg-Cohen N, Miller NR, Repka MX. Traumatic optic neuropathy in children and adolescents. J AAPOS. Feb 2004;8(1):20-7. [Medline].
15. Holmes MD, Sires BS. Flash visual evoked potentials predict visual outcome in traumatic optic neuropathy. Ophthal Plast Reconstr Surg. Sep 2004;20(5):342-6. [Medline].
16. Kountakis SE, Maillard AA, El-Harazi SM, et al. Endoscopic optic nerve decompression for traumatic blindness. Otolaryngol Head Neck Surg. Jul 2000;123(1 Pt 1):34-7. [Medline].
17. Levin LA, Beck RW, Joseph MP, et al. The treatment of traumatic optic neuropathy: the International Optic Nerve Trauma Study. Ophthalmology. Jul 1999;106(7):1268-77. [Medline].
18. Li KK, Teknos TN, Lauretano A, et al. Traumatic optic neuropathy complicating facial fracture repair. J Craniofac Surg. Sep 1997;8(5):352-5; discussion 356-9. [Medline].
19. Medeiros FA, Moura FC, Vessani RM, et al. Axonal loss after traumatic optic neuropathy documented by optical coherence tomography. Am J Ophthalmol. Mar 2003;135(3):406-8. [Medline].
20. Medeiros FA, Susanna R Jr. Retinal nerve fiber layer loss after traumatic optic neuropathy detected by scanning laser polarimetry. Arch Ophthalmol. Jun 2001;119(6):920-1. [Medline].
21. Miyahara T, Kurimoto Y, Kurokawa T, et al. Alterations in retinal nerve fiber layer thickness following indirect traumatic optic neuropathy detected by nerve fiber analyzer, GDx-N. Am J Ophthalmol. Aug 2003;136(2):361-4. [Medline].
22. Ohlsson M, Westerlund U, Langmoen IA, et al. Methylprednisolone treatment does not influence axonal regeneration or degeneration following optic nerve injury in the adult rat. J Neuroophthalmol. Mar 2004;24(1):11-8. [Medline].
23. Rajiniganth MG, Gupta AK, Gupta A, et al. Traumatic optic neuropathy: visual outcome following combined therapy protocol. Arch Otolaryngol Head Neck Surg. Nov 2003;129(11):1203-6. [Medline].
24. Steinsapir KD, Goldberg RA. Traumatic optic neuropathy. Surv Ophthalmol. May-Jun 1994;38(6):487-518. [Medline].
25. Sucher NJ, Lipton SA, Dreyer EB. Molecular basis of glutamate toxicity in retinal ganglion cells. Vision Res. Dec 1997;37(24):3483-93. [Medline].
26. Tsai HH, Jeng SF, Lin TS, et al. Predictive value of computed tomography in visual outcome in indirect traumatic optic neuropathy complicated with periorbital facial bone fracture. Clin Neurol Neurosurg. Apr 2005;107(3):200-6. [Medline].
27. Wang BH, Robertson BC, Girotto JA, et al. Traumatic optic neuropathy: a review of 61 patients. Plast Reconstr Surg. Jun 2001;107(7):1655-64. [Medline].
28. Yip CC, Chng NW, Au Eong KG, et al. Low-dose intravenous methylprednisolone or conservative treatment in the management of traumatic optic neuropathy. Eur J Ophthalmol. Jul-Aug 2002;12(4):309-14. [Medline].
29. Yu Wai Man P, Griffiths PG. Surgery for traumatic optic neuropathy. Cochrane Database Syst Rev. Oct 19 2005;CD005024. [Medline].
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Article Last Updated: Jul 28, 2008