Traumatic Optic Neuropathy

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Traumatic Optic Neuropathy

Disease Entity


Traumatic Optic Neuropathy (TON) is a condition in which acute injury to the optic nerve from direct or indirect trauma results in vision loss. The severity of optic nerve damage may range from simple contusion to complete avulsion of the optic nerve.


The most common cause of TON is indirect injury to the optic nerve, which is thought to be the result of transmitted shock from an orbital impact to the intracanalicular portion of optic nerve. Direct TON can result from penetrating injury or from bony fragments in the optic canal or orbit piercing the optic nerve. Orbital hemorrhage (orbital compartment syndrome) and optic nerve sheath hematoma can also cause TON by direct compression.

Risk Factors

A CT scan of a patient found to have traumatic optic neuropathy of the left eye. Note that this patient has a left Le Fort 3 fracture with a left superior orbital roof fracture. The medial and inferior wall of the left orbit are also fractured.

There are no known risk factors for TON. In the International Optic Nerve Trauma Study, 85% of patients with indirect TON were male, and the average age of patients with TON was 34.[1] The most common mechanisms of injury were motor vehicle accident, bike accident, fall and assault. While abusive injury is a rare cause of TON, it is an important concern in infants.

General Pathophysiology

The exact pathophysiology of indirect TON is not well understood. The optic nerve dura is continuous with the orbital periosteum, leaving the optic nerve susceptible to transmission of force from blunt head trauma, particularly that affecting the superior orbital rim. Indirect TON has been hypothesized to result from shearing injury to the intracanalicular portion of optic nerve, which can cause axonal injury or disturb the blood supply of the optic nerve. It has also been suggested that the optic nerve may swell in the optic canal after trauma resulting in increased luminal pressure and secondary ischemic injury. Retinal ganglion cell loss can also occur soon after injury. Direct TON is presumed to be the result of tissue disruption secondary to foreign body or bony fragments impacting the optic nerve directly.

Primary prevention

There is no primary prevention for TON. 


The diagnosis of TON is made clinically based on history and ophthalmic signs. Like other optic neuropathies, patients with TON may have decreased central visual acuity, decreased color vision, an afferent pupillary defect and/or visual field deficits. It is important to remember that albeit rare, TON can be bilateral, so a relative afferent pupillary defect may not be seen in patients with bilateral injury and vision loss. The optic nerve head may will appear normal initially, and optic atrophy can be seen 3-6 weeks after the initial traumatic event.


A history consistent with TON is vision loss immediately or shortly after blunt or penetrating head trauma. Patients may report acute unilateral decrease in vision, color vision deficits, and/or visual field deficits. The history and subjective complaints may be delayed due to the impact of and treatment for other concomitant head injuries or other systemic injuries.


  • Vision loss
  • Visual field defects
  • Decreased color perception

Physical examination

The initial external eye exam may show signs of orbital trauma or fracture (soft tissue edema, hematoma, ecchymoses, step-off on palpation of orbital rim). Decreased visual acuity and a relative afferent pupillary defect (in unilateral cases) are also seen. On funduscopy, the initial optic nerve head assessment may be normal, but signs of optic atrophy may be seen 3-6 weeks after trauma.


  • Decreased visual acuity
  • Decreased color vision
  • Afferent pupillary defect
  • Visual field deficits

Clinical diagnosis

The clinical diagnosis of TON is made on the basis of a specific constellation of history and physical exam findings. Patients have a history of trauma, and complain of or are found to have significant visual loss, decreased color vision, visual field deficit, afferent pupillary defect. Dilated fundus exam is often unremarkable initially.

Diagnostic procedures

The diagnosis of TON is primarily clinical. There are some tests that can aid in the management and diagnosis of TON. It is important to obtain neuroimaging, usually a CT of the orbit with coronal and axial thin sections (1 mm) through the optic canal are crucial to visualize the optic nerve as well as the optic canal and carefully evaluate for evidence of fracture. This can help assess for compression of the optic nerve by a hematoma or bony fragments impinging on the optic nerve, which would require urgent surgical intervention. Automated visual field testing such as a Humphrey (HVF) can be used to characterize visual field defects/scotomas in patients with TON, if acuity remains adequate for such testing. Finally, a visual evoked potential (VEP) can be used to characterize the electrical activity of the optic nerve.

Laboratory test

There are no laboratory tests to aid in the diagnosis of TON.

Differential diagnosis

  • Posterior ischemic optic neuropathy
  • Optic neuritis
  • Optic nerve avulsion
  • Non-organic vision loss
  • Pre-/intra-/subretinal hemorrhage
  • Choroidal Rupture
  • Commotio retinae


Aside from observation, the two treatment options widely practiced include high-dose corticosteroids or surgical decompression.[2] The management of TON is controversial, and so far, data in the literature have not shown any treatment to be superior to observation.[1][3]

Medical therapy

Some authors have supported the use of high or “mega" dose corticosteroids in TON. This therapeutic regimen has been extrapolated from the National Acute Spinal Cord Injury Study II, which showed a statistically significant improvement in neurologic outcome (motor and sensory) in a subgroup analysis of acute spinal cord injury patients receiving a methyprednisolone 30 mg/kg bolus within eight hours of injury, followed by 5.4 mg/kg/hr for 23 hours.[4] Subsequently however, the CRASH (Corticosteroid Randomization After Significant Head injury) study showed an increased relative risk (1.05, P=0.079) of death in patients given this regimen after significant head injury.[5] The International Optic Nerve Trauma Study also did not show a difference in final visual acuity between patients with TON that were observed only compared with those given steroids.[1] Therefore, "megadose" steroids are now considered to be contraindicated in this setting. High dose steroids can be considered on a case-by-case basis.

There are a number of other experimental techniques that may be considered for use in the future. Mouse models have shown promising results in reducing retinal ganglion cell loss with the use of resveratrol, an antioxidant with neuroprotective effects, after optic nerve crush injury.[6] Other studies by Entezari et al. and Kashkouli et al. reported visual improvement in patients treated with erythropoietin, which has previously been shown to have neuroprotective effects.[7][8]


Surgical decompression of the optic nerve for TON has been used as an alternative to observation and high-dose corticosteroid therapy. In theory, removing structures that surround the intracanalicular optic nerve decompresses the nerve, thereby alleviating ischemic changes.[2] This is usually performed by an otolaryngologist or neurosurgeon using an intranasal endoscopic or transcranial approach, and the results are generally unsatisfactory if performed more than 2 weeks after the injury.[2] Some have supported the use of surgery in certain cases, such as when a bony fragment is abutting to optic nerve or in the case of an optic nerve sheath hematoma, but there is not strong data to support surgery as a superior option for indirect TON. Additionally, surgical intervention for TON was not shown to be beneficial over steroids or observation in The International Optic Nerve Trauma Study.[1]


Serious surgical complications specific to decompression surgery for TON include infection (meningitis), CSF leaks, and exacerbation of traumatic optic neuropathy. Complications from high or “mega” dose steroids include wound infection, a wide number of systemic adverse effects (i.e. GI bleed), and increased risk of death.


Prognosis is dependent on the extent of injury to the optic nerve. In the International Optic Nerve Trauma Study, patients with NLP vision failed to improve as often as those with better vision. This study also showed that visual acuity improvement of >3 lines on the Snellen chart was seen in 57% of the untreated group, 52% of the group that received steroids alone, and 32% of the group that underwent surgery; however, these results were not statistically different (P=0.22).[1]

Additional Resources


  1. 1.0 1.1 1.2 1.3 1.4 Levin, L.A., et al., The treatment of traumatic optic neuropathy: the International Optic Nerve Trauma Study. Ophthalmology, 1999. 106(7): p. 1268-77.
  2. 2.0 2.1 2.2 He Z, Li Q, Yuan J, et al. Evaluation of transcranial surgical decompression of the optic canal as a treatment option for traumatic optic neuropathy. Clin Neurol Neurosurg. Jul 2015;134:130-5. doi:10.1016/j.clineuro.2015.04.023
  3. Wladis EJ, Aakalu VK, Sobel RK, McCulley TJ, Foster JA, Tao JP, Freitag SK, Yen MT. Interventions for Indirect Traumatic Optic Neuropathy: A Report by the American Academy of Ophthalmology. Ophthalmology. 2020 Nov 6:S0161-6420(20)31041-1. doi: 10.1016/j.ophtha.2020.10.038. Epub ahead of print. PMID: 33161071.
  4. Young, W., NASCIS. National Acute Spinal Cord Injury Study. J Neurotrauma, 1990. 7(3): p. 113-4.
  5. Edwards, P., 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, 2005. 365(9475): p. 1957-9.
  6. Zuo, et al. SIRT1 promotes RGC survival and delays loss of function following optic nerve crush. Invest Ophthalmol Vis Sci. 2013 26;54(7):5097-102
  7. Entezari M, Esmaeili M, Yaseri M. A pilot study of the effect of intravenous erythropoetin on improvement of visual function in patients with recent indirect traumatic optic neuropathy. Graefes Arch Clin Exp Ophthalmol. Aug 2014;252(8):1309-13. doi:10.1007/s00417-014-2691-6
  8. Kashkouli MB, Pakdel F, Sanjari MS, et al. Erythropoietin: a novel treatment for traumatic optic neuropathy-a pilot study. Graefes Arch Clin Exp Ophthalmol. May 2011;249(5):731-6. doi:10.1007/s00417-010-1534-3