Traumatic Optic Neuropathy

From EyeWiki

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 concerns in infants.

General Pathology

The exact pathology 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. Direct TON is presumed to be the result of tissue disruption secondary to foreign body or bony fragments impacting on the optic nerve.

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 an afferent pupillary defect may not be seen in patients with bilateral injury and vision loss. The optic nerve head will appear normal initially, but optic atrophy can be seen 3-6 weeks after the initial traumatic event.


A history consistent with TON would be vision loss after blunt or penetrating trauma that could not be explained by slit lamp or dilated fundus findings. Often these patients complain of acute unilateral decrease in vision, color vision deficits, 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 comorbidities.


  • Blurry vision
  • Scotomas and visual field defect
  • Decreased color sensation

Physical examination

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


  • Decreased Vision
  • Decreased color vision (Dyschromatopsia)
  • 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, an afferent papillary defect, and a dilated fundus exam negative to explain these signs.

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 evaluated 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 surgical intervention. Automated visual field testing such as a Humphrey (HVF) can be usually to characterize visual field defects/scotomas in patients with TON over time. Finally, a 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


The management of TON is controversial, however, the data in the literature to date has not shown any treatment to be superior to observation[2].

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,.[3] Subsequently however,the CRASH (Corticosteroid Randomization After Significant Head injury) study showed an increased relative risk of death in patients given this regimen after significant head injury.[4] The International Optic Nerve Trauma Study also did not show a difference in final visual acuity between patients with TON that were observed compared with those given steroids.[1] Mouse models have shown promising results with the use of resveratrol after optic nerve crush injury. [5]


Surgical intervention for TON was shown to not be beneficial in The International Optic Nerve Trauma Study. Some have supported the use of surgery in certain scenarios such as when a bony fragment is abutting to optic nerve or in the case of an optic nerve sheath hematoma but there is no good data supporting surgery for indirect TON.


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 and GI bleed.


In the International Optic Nerve Trauma Study, visual acuity improvement of >3 lines was seen in 57% of the untreated group, 52% of the group that received steroids alone, and 32% of the group that underwent surgery. This was not a statistically significant result.

Additional Resources


  1. 1.0 1.1 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. 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.
  3. Young, W., NASCIS. National Acute Spinal Cord Injury Study. J Neurotrauma, 1990. 7(3): p. 113-4.
  4. 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.
  5. 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
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