Traumatic Optic Neuropathy

Original Editor - Momina Khalid Top Contributors - Momina Khalid

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 in Traumatic optic neuropathy may range from a simple contusion to a complete avulsion of the optic nerve.

Traumatic Optic Neuropathy

Etiology

The most common cause of Traumatic optic neuropathy 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 the optic nerve.

Classification

Traumatic optic neuropathy is classified as direct or indirect.

Direct TON

Direct Traumatic optic neuropathy usually presents as severe visual loss with minimal chances for recovery. It is caused by a penetrating injury to the area of optic nerve.

Indirect TON

Indirect Traumatic optic neuropathy is caused by acceleration/deceleration forces due to blunt head or closed globe trauma. The vision loss may vary from mild to total blindness. On clinical examination, the retina and optic nerve head look normal

Pathophysiology

Following trauma, there is an immediate shearing of a proportion of retinal ganglion cell axons, an irreversible process that results in neuronal loss. There is then a degree of optic nerve swelling within the tight confines of the optic canal, secondary to direct mechanical trauma and vascular ischemia. The ensuing compartment syndrome further impairs the already compromised blood supply to surviving retinal ganglion cells, setting up a downward spiral toward apoptotic cell death.

Risk Factors

There are no known specific risk factors for Traumatic optic neuropathy . However, it is important to note that Traumatic optic neuropathy (and trauma in general) predominantly affects younger males

The most common mechanisms of injury in TON include

• motor vehicle accidents,
• bike accidents,
• falls, and
• assaults.

While abusive injury is a rare cause of Traumatic optic neuropathy, it is an important concern in infants.

Diagnosis

Traumatic optic neuropathy is a clinical diagnosis that can be supported by radiographic evaluation in patients with a history of craniofacial blunt injury. Like other optic neuropathies, patients with Traumatic optic neuropathy 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, Traumatic optic neuropathy 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 appear normal initially, and optic atrophy can be seen 3-6 weeks after the initial traumatic event.

Signs & Symptoms

Symptoms

• Vision loss
• Visual field defects
• Decreased color perception

Signs

• Decreased visual acuity
• Decreased color vision
• Afferent pupillary defect
• Visual field deficits
• Optic disc edema but often a normal optic nerve initially (retrobulbar optic neuropathy) followed by optic atrophy later

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 fundoscopy, the initial optic nerve head assessment may be normal, but signs of optic atrophy may be seen 3-6 weeks after trauma. Clinicians should exclude a penetrating or perforating globe injury in cases of presumed Traumatic optic neuropathy .

Differential diagnosis

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

Management

The management of Traumatic optic neuropathy is controversial, however, the data in the literature to date has not shown any treatment to be superior to observation.

Medical therapy

Some authors have supported the use of high- or "mega" dose corticosteroids in Traumatic optic neuropathy . 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,. 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. The International Optic Nerve Trauma Study also did not show a difference in final visual acuity between patients with Traumatic optic neuropathy that were observed compared with those given steroids.

Surgery

Surgical intervention for Traumatic optic neuropathy 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 toheoptic nerve or in the case of an optic nerve sheath hematoma but there is no good data supporting surgery for indirect TON.

Complications

Serious surgical complications specific to decompression surgery for Traumatic optic neuropathy include

• infection (meningitis)
• CSF leaks
• exacerbation of traumatic optic neuropathy
• Complications from high-dose steroids include wound infection and Gl bleed.